Enlargement of the HEART due to chamber HYPERTROPHY, an increase in wall thickness without an increase in the number of cells (MYOCYTES, CARDIAC). It is the result of increase in myocyte size, mitochondrial and myofibrillar mass, as well as changes in extracellular matrix.
| Excerpt | Reference |
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| "Development of cardiac hypertrophy is associated with depletion of endogenous catecholamine stores and increased inotropic response to exogenous catecholamines." | ( Limas, CJ, 1979) |
| "Cardiac hypertrophy is an adaptive response to an increased load imposed on the myocyte which allows the heart to perform increased work while maintaining normal myocardial fiber stress and shortening in systole." | ( Lorell, BH, 1992) |
| "Cardiac hypertrophy is associated with impaired coronary vasodilator and chronotropic responsiveness to serotonin." | ( Mertens, MJ; Pfaffendorf, M; van Zwieten, PA, 1992) |
| "Whether cardiac hypertrophy is a compensatory response or a cause of decompensation has been an interesting and important controversy in cardiology." | ( Honda, M; Ishikawa, S; Ishinaga, Y; Morioka, S; Moriyama, K; Tanaka, K; Yano, S, 1992) |
| "Cardiac hypertrophy is characterized by marked abnormalities in the contraction/relaxation pattern of the heart." | ( Neyses, L; Vetter, H, 1990) |
| "The development of cardiac hypertrophy is associated with marked changes in cardiac autonomic innervation." | ( Lindpaintner, K; Lund, DD; Schmid, PG, 1987) |
| "Regression of cardiac hypertrophy is possible by differentiated pharmacotherapy, e." | ( Strauer, BE, 1985) |
| "Cardiac hypertrophy is accompanied by a significant reduction in the number of phorbol ester receptors on enzymatically dissociated myocytes with no changes in their affinities." | ( Limas, C; Limas, CJ, 1986) |
| "Even though cardiac hypertrophy is viewed as a beneficial compensatory process that normalizes wall stress, the increased muscle mass carries with it the need of increased blood supply." | ( Burkart, F; Kiowski, W, 1988) |
| "Cardiac hypertrophy is frequently associated with sympathetic changes that include increased myocardial norepinephrine turnover, depleted myocardial norepinephrine stores, decreased myocardial responses to sympathetic nerve stimulation, and elevated plasma catecholamines." | ( Siri, FM, 1988) |
| "However, if cardiac hypertrophy is left unattended beyond a certain period, physiological hypertrophy is converted to pathological hypertrophy whereby the cardiac muscle is unable to generate an adequate amount of contractile activity." | ( Beamish, RE; Dhalla, NS; Heyliger, CE; Innes, IR, 1987) |
| "Cardiac hypertrophy is associated with a decrease in coronary reserve." | ( Marcus, ML; Peters, KG; Tomanek, RJ; Wangler, RD, 1982) |
| "Cardiac hypertrophy is known to be associated with reductions in cellular cAMP." | ( Rabkin, SW, 1993) |
| "Pressure-overload cardiac hypertrophy is associated with the re-expression of an ensemble of genes representative of embryonic myocardium, whose protein products modulate myocardial function." | ( Parker, TG, 1995) |
| "Cardiac hypertrophy is commonly observed in acromegalic patients, in whom serum insulin-like growth factor-I (IGF-I) levels are elevated." | ( Adachi, S; Hirata, Y; Hiroe, M; Ito, H; Koike, A; Marumo, F; Nogami, A; Shichiri, M; Tsujino, M, 1993) |
| "Hypertensive cardiac hypertrophy is associated with collagen accumulation in the myocardial interstitium." | ( Sano, H, 1994) |
| "Because cardiac hypertrophy is a significant independent risk factor for cardiovascular morbidity and mortality, it is important to understand this dissociation between blood pressure and cardiac enlargement and also to consider the possible impact of such findings on the clinical use of minoxidil." | ( Cifani, JR; Khairallah, PA; Milovanovic, M; Moravec, CS; Ruhe, T, 1994) |
| "The degree of cardiac hypertrophy is not only load dependent: Among other factors, the renin-angiotensin system may play a role in the regulation of cardiac myocyte growth." | ( Harmsen, E; Leenen, FH; Ruzicka, M; Yuan, B, 1993) |
| "Cardiac hypertrophy is the physiological adaptation of the heart to chronic mechanical overload." | ( Charlemagne, D; Chevalier, B; Mansier, P; Moalic, JM; Swynghedauw, B, 1993) |
| "Although cardiac hypertrophy is reported to be induced in rats by a fat-free diet, little is known of the consequences of depressed myocardial long-chain fatty acid uptake." | ( Kawamura, K; Kusaka, Y; Matsunaga, Y; Miyazaki, H; Okamoto, F; Tanaka, T; Terasaki, F, 1995) |
| "Thus cardiac hypertrophy is characterized by an abundant 120 kDa cytosolic tyr phos protein, which is apparent with Ang II stimulation in milder degrees of cardiac hypertrophy, and is most likely an as yet uncharacterized protein." | ( Damen, JE; Goutsouliak, V; Krystal, G; Rabkin, SW, 1996) |
| "Cardiac hypertrophy is associated with altered expression of the components of the cardiac renin-angiotensin system (RAS)." | ( Lee, MA; Lee, YA; Liang, CS; Lindpaintner, K, 1996) |
| "Hypertensive cardiac hypertrophy is associated with the accumulation of collagen in the myocardial interstitium." | ( Kawaguchi, H; Kitabatake, A, 1996) |
| "Cardiac hypertrophy is a commonly observed complication of a variety of cardiovascular diseases." | ( Ito, H, 1997) |
| "Hypertensive cardiac hypertrophy is associated with the accumulation of collagen in the myocardial interstitium." | ( Iizuka, K; Kawaguchi, H; Kitabatake, A; Murakami, T; Okamoto, H; Sano, H, 1998) |
| "We show that cardiac hypertrophy is induced by the calcium-dependent phosphatase calcineurin, which dephosphorylates the transcription factor NF-AT3, enabling it to translocate to the nucleus." | ( Antos, CL; Grant, SR; Lu, JR; Markham, B; Molkentin, JD; Olson, EN; Richardson, J; Robbins, J, 1998) |
| "Cardiac hypertrophy is an adaptive response that normalizes wall stress and compensates for increased workload." | ( Hefti, MA; Morano, I; Schaub, MC; Zuellig, RA, 1998) |
| "Cardiac hypertrophy is frequent in chronic hypertension." | ( Aubert, JF; Brunner, DB; Brunner, HR; Gabbiani, G; Mazzolai, L; Nussberger, J; Pedrazzini, T, 1998) |
| "Whether cardiac hypertrophy is present and even more pronounced in peripheral vascular disease than in other populations has never been explored." | ( Brahimi, M; Dabiré, H; Levy, BI; Safar, ME, 1998) |
| "Cardiac hypertrophy is associated with modifications in Ca2+ transport processes, enzymes of energy metabolism and antioxidant capacity." | ( Geil, D; Günther, J; Lammerich, A; Pfitzer, G; Schimke, I; Stauss, HM; Theres, H; Vetter, R; Wagner, KD, 1998) |
| "Cardiac hypertrophy is an adaptive response of the heart to a variety of intrinsic and extrinsic stimuli." | ( McKinsey, TA; Olson, EN, 1999) |
| "Cardiac hypertrophy is a fundamental adaptive response to hemodynamic overload; how mechanical load induces cardiac hypertrophy, however, remains elusive." | ( Hayashi, D; Komuro, I; Kudoh, S; Nagai, R; Oka, T; Shibasaki, F; Shimoyama, M; Takimoto, E; Uozumi, H; Yazaki, Y; Zou, Y, 1999) |
| "Cardiac hypertrophy is a major predictor of future morbidity and mortality." | ( De Windt, LJ; Lim, HW; Molkentin, JD; Taigen, T, 2000) |
| "Cardiac hypertrophy is an adaptive process to an increased hemodynamic overload." | ( Yamazaki, T; Yazaki, Y, 2000) |
| "Cardiac hypertrophy is considered a necessary compensatory response to sustained elevations of left ventricular (LV) wall stress." | ( Davisson, RL; Hill, JA; Karimi, M; Kerber, RE; Kutschke, W; Wang, Z; Weiss, RM; Zimmerman, K, 2000) |
| "Cardiac hypertrophy is associated with specific alterations in myocardial gene expression; however, the exact mechanisms responsible for altered gene expression are poorly defined." | ( Babu, GJ; Lalli, MJ; Periasamy, M; Sadoshima, J; Sussman, MA, 2000) |
| "Cardiac hypertrophy is a major predictor of heart failure and of morbidity and mortality in developed countries." | ( Böhm, M; Geisler, M; Mies, F; Nohr, T; Schnabel, P, 2000) |
| "Cardiac hypertrophy is characterized by both remodeling of the extracellular matrix (ECM) and hypertrophic growth of the cardiocytes." | ( Cooper, G; Jiang, W; Kuppuswamy, D; Laser, M; Menick, DR; Willey, CD; Zile, MR, 2000) |
| "Cardiac hypertrophy is characterized by increased cardiomyocyte protein synthesis, increased cell volume, and a shift in cardiac-specific gene expression to fetal isoforms." | ( Abe, S; Adachi, S; Hiroe, M; Ito, H; Marumo, F; Nozato, T; Ono, Y; Tamamori, M, 2000) |
| "Cardiac hypertrophy is a major problem in cardiac diseases, so the present study was designed to elucidate the effects of sarpogrelate on cardiac hypertrophy." | ( Harada, M; Hosoya, T; Ikeda, K; Nakao, K; Tojo, K; Tokudome, G, 2000) |
| "Cardiac hypertrophy is a compensatory response of myocardial tissue upon increased mechanical load." | ( Ruwhof, C; Schrier, PI; van der Laarse, A; van der Valk-Kokshoom, LE; van Wamel, AJ, 2001) |
| "Cardiac hypertrophy is one of the serious complications which increase mortality due to cardiovascular diseases." | ( Adachi, S; Hiroe, M; Ito, H; Marum, F; Nozato, T; Ono, Y; Sunamori, M; Tanaka, H; Watanabe, M, 2001) |
| "Cardiac hypertrophy is associated with elevated plasma catecholamine levels and an increase in cardiac morbidity and mortality." | ( Caron, K; Esposito, G; Mao, L; Rapacciuolo, A; Rockman, HA; Thomas, SA, 2001) |
| "Cardiac hypertrophy is an independent risk factor for cardiovascular morbidity and mortality in men and in women." | ( Cleutjens, JP; Doevendans, PA; Grohé, C; Janssen, BJ; van Eickels, M; Wellens, HJ, 2001) |
| "Cardiac hypertrophy is common in hypertension but its development is influenced by angiotensin II, sodium intake aldosterone, and the time of day blood pressure (BP) is elevated." | ( Aubert, JF; Brunner, H; Morgan, T, 2001) |
| "Cardiac hypertrophy is a major cause of morbidity and mortality worldwide." | ( Grimm, M; Kitakaze, M; Liao, JK; Liao, Y; Nakagami, H; Node, K; Takemoto, M; Takemoto, Y, 2001) |
| "Cardiac hypertrophy is associated with increased incidence of sudden death and susceptibility to proarrhythmic effects of antiarrhythmic agents." | ( El-Sherif, N; Kozhevnikov, DO; Restivo, M; Robotis, D; Yamamoto, K, 2002) |
| "Cardiac hypertrophy is an adaptive response to a variety of mechanical and hormonal stimuli, and represents an early event in the clinical course leading to heart failure." | ( Altruda, F; Brancaccio, M; De Acetis, M; Fratta, L; Guazzone, S; Hirsch, E; Lembo, G; Marino, G; Notte, A; Poulet, R; Silengo, L; Tarone, G; Vecchione, C, 2003) |
| "Cardiac hypertrophy is the consequence of hypertrophic stimulus-induced changes in gene expression, which is linked by intracellular signal transduction." | ( Fu, MG; Tang, CS, 2000) |
| "Cardiac hypertrophy is characterized by remodeling of the extracellular matrix (ECM)." | ( Chun, JS; Kim, DJ; Kim, JK; Lim, CS; Park, SH; Song, WK, 2003) |
| "Cardiac hypertrophy is a common and often lethal complication of arterial hypertension." | ( Baba, HA; Begrow, F; Bubikat, A; Garbers, DL; Holtwick, R; Kuhn, M; Schneider, MD; Skryabin, BV; van Eickels, M, 2003) |
| "Cardiac hypertrophy is induced by a number of stimuli and can lead to cardiomyopathy and heart failure." | ( Busk, PK; Enevoldsen, M; Haunsø, S; Sheikh, SP; Strøm, CC; Thirstrup, K; Wulf-Andersen, L, 2003) |
| "Cardiac hypertrophy is often associated with an increased sympathetic drive, and both in vitro and in vivo studies have demonstrated the development of cardiomyocyte hypertrophy in response to either alpha- or beta-adrenergic stimulation." | ( Camihort, G; Camilión de Hurtado, MC; Cingolani, HE; Console, GM; Dumm, CG; Ennis, IL; Escudero, EM; Seidler, RW, 2003) |
| "Cardiac hypertrophy is an adaptive response to increases in blood pressure." | ( Liao, JK; Nakagami, H; Takemoto, M, 2003) |
| "Cardiac hypertrophy is an early phenotypic manifestation of the AhR knockout." | ( Atallah-Yunes, N; Chase, SE; Silverstone, AE; Smith, FC; Vasquez, A; Vikstrom, KL; You, X, 2003) |
| "Cardiac hypertrophy is an initial physiological adaptive response by the heart to pressure overload." | ( Jensen, KS; Liao, JK; Nakagami, H, 2003) |
| "Cardiac hypertrophy is an early landmark during the clinical course of heart failure, and is an important risk factor for subsequent morbidity and mortality." | ( Arcilla, R; Gupta, M; Ilbawi, M; Ingram, P; Ocampo, C, 2003) |
| "Cardiac hypertrophy is observed in the majority of patients with chronic renal failure undergoing haemodialysis." | ( Arimoto, T; Ito, M; Konta, T; Kubota, I; Miyamoto, T; Miyashita, T; Shishido, T; Takahashi, H; Takeishi, Y, 2004) |
| "Cardiac hypertrophy is characterized by increased cardiomyocyte size, mRNA levels for atrial natriuretic factor (ANF), and protein synthesis." | ( Dhalla, NS; Singal, T; Tappia, PS, 2004) |
| "Cardiac hypertrophy is formed in response to hemodynamic overload." | ( Harada, K; Hayashi, D; Imai, Y; Komuro, I; Kudoh, S; Monzen, K; Nagai, R; Shimoyama, M; Shiojima, I; Yamazaki, T; Yazaki, Y; Zou, Y, 2004) |
| "Cardiac hypertrophy is a leading predicator of progressive heart disease that often leads to heart failure and a loss of cardiac contractile performance associated with profound alterations in intracellular calcium handling." | ( Molkentin, JD; Wilkins, BJ, 2004) |
| "Cardiac hypertrophy is a major cause of morbidity and mortality worldwide." | ( Hao, DL; Huang, Y; Hui, RT; Li, HL; Liang, CC; Lin, M; Liu, DP; Liu, G; Liu, YQ; Wang, AB; Wei, C; Williams, GM; Zhang, CN, 2005) |
| "Cardiac hypertrophy is a complex and nonhomogenous response to various stimuli." | ( Bodyak, N; Brown, J; Izumo, S; Kang, PM; Kong, SW; Liu, Z; Yue, P, 2005) |
| "Cardiac hypertrophy is triggered in response to mechanical stress and various neurohumoral factors, such as G-protein coupling receptor (GPCR) and gp130 cytokine receptor agonists." | ( Hoshijima, M; Iwata, M; Kuroda, S; Maturana, A; Okajima, T; Tanizawa, K; Tatematsu, K; Van Lint, J; Vandenheede, JR, 2005) |
| "Cardiac hypertrophy is an independent risk factor predictive of cardiovascular disease and is significantly associated with morbidity and mortality." | ( Curl, CI; Delbridge, LM; Domenighetti, AA; Huggins, CE; Morgan, TO; Pedrazzini, T; Porrello, ER, 2004) |
| "Cardiac hypertrophy is a compensatory response to increased mechanical load." | ( Abassi, Z; Barac, YD; Binah, O; Coleman, R; Milman, F; Reiter, I; Shilkrut, M; Yaniv, G; Zeevi-Levin, N, 2005) |
| "Cardiac hypertrophy is considered as an independent risk factor associated with abnormalities of diastolic function and can result in heart failure." | ( Godfraind, T, 2006) |
| "Cardiac hypertrophy is a response of the heart to a wide range of extrinsic stimuli, such as arterial hypertension, valvular heart disease, myocardial infarction, and cardiomyopathy." | ( Calvo, RR; Planavila, A; Vázquez-Carrera, M, 2006) |
| "Pathological cardiac hypertrophy is considered a precursor to clinical heart failure." | ( Chin, MT; Cui, L; Liao, JK; Liao, R; Nakagami, H; Sakata, Y; Xiang, F; Youngblood, JM, 2006) |
| "The development of cardiac hypertrophy is mediated, in part, by increase in NADPH oxidase activity and myocardial oxidative stress." | ( Kwiatkowski, DJ; Liao, JK; Mukai, Y; Ogita, H; Satoh, M; Takeshita, K, 2006) |
| "The role of AMPK in cardiac hypertrophy is also controversial." | ( Dyck, JR; Lopaschuk, GD, 2006) |
| "Cardiac hypertrophy is a major cause of morbidity and mortality worldwide." | ( Huang, Y; Hui, RT; Li, HL; Liang, CC; Liu, DP; Liu, G; Liu, YQ; Wang, AB; Wei, C; Wei, YS; Williams, GM; Zhang, CN, 2006) |
| "Cardiac hypertrophy is an adaptive process to an increased hemodynamic overload." | ( Guo, WG; Xie, MJ; Yu, ZB, 2006) |
| "Cardiac hypertrophy is an adaptive process against increased work loads; however, hypertrophy also presents substrates for lethal ventricular arrhythmias, resulting in sudden arrhythmic deaths that account for about one third of deaths in cardiac hypertrophy." | ( Furukawa, T; Kurokawa, J, 2006) |
| "Cardiac hypertrophy is an established and independent risk factor for the development of heart failure and sudden cardiac death." | ( Liao, R; Lim, CC; Yang, M; Zhang, X, 2007) |
| "Cardiac hypertrophy is an independent predictor of cardiovascular morbidity and mortality." | ( Abriel, H; Boixel, C; Cefai, D; Domenighetti, AA; Pedrazzini, T, 2007) |
| "To examine whether cardiac hypertrophy is associated with changes in beta-adrenoceptor signal transduction mechanisms, pressure overload (PO) was induced by occlusion of the abdominal aorta and volume overload (VO) by creation of an aortocaval shunt for 4 and 24 wk in rats." | ( Dhalla, NS; Elimban, V; Guo, X; Saini, HK; Sethi, R; Wang, X, 2007) |
| "Cardiac hypertrophy is associated with a dramatic change in the gene expression profile of cardiac myocytes." | ( Bingham, AJ; Kozera, L; Ooi, L; White, E; Wood, IC, 2007) |
| "Pathological cardiac hypertrophy is associated with the expression of a gene profile reminiscent of foetal development." | ( Catalano, L; Fasanaro, P; Marano, G; Musumeci, M; Palazzesi, S; Patrizio, M; Stati, T, 2007) |
| "Heart hypertrophy is a common finding of acromegaly, a syndrome due to GH excess." | ( Bartalena, L; Bogazzi, F; D'Alessio, A; Fanelli, G; Gasperi, M; Manariti, A; Martino, E; Raggi, F; Russo, D; Ultimieri, F; Viacava, P, 2007) |
| "Cardiac hypertrophy is a major cause of human morbidity and mortality." | ( Glass, DJ; Li, HH; Lockyer, P; McDonough, H; Miller, N; Patterson, C; Willis, MS, 2007) |
| "Cardiac hypertrophy is a common pathological change accompanying cardiovascular disease." | ( Li, HZ; Lin, Y; Lv, YJ; Tian, Y; Wang, C; Wang, LN; Xi, YH; Xu, CQ; Yang, BF; Zhang, WH; Zhao, YJ, 2008) |
| "Cardiac hypertrophy is induced by various stresses such as hypertension and myocardial infarction." | ( Kurose, H; Nishida, M, 2008) |
| "Pathophysiological cardiac hypertrophy is one of the most common causes of heart failure." | ( Ai, D; Chiamvimonvat, N; Hammock, BD; Jones, PD; Li, N; Pang, W; Shyy, JY; Xu, M; Yang, J; Zhang, Y; Zhu, Y, 2009) |
| "Cardiac hypertrophy is associated with alterations in cardiomyocyte excitation-contraction coupling (ECC) and Ca(2+) handling." | ( Delbridge, LM; Domenighetti, AA; Egger, M; Gusev, K; Niggli, E; Pedrazzini, T, 2009) |
| "Cardiac hypertrophy is a growth response of the heart to increased hemodynamic demand or damage." | ( Bootman, MD; Conway, SJ; Foo, RS; Harzheim, D; Movassagh, M; Ritter, O; Roderick, HL; Tashfeen, A, 2009) |
| "Cardiac hypertrophy is associated with a reduction in the contractile response to beta-adrenergic stimulation, and with re-expression of foetal genes such as beta-myosin heavy chain (MHC)." | ( Pandya, K; Porter, K; Rockman, HA; Smithies, O, 2009) |
| "Cardiac hypertrophy is accompanied by maladaptive cardiac remodeling, which leads to heart failure or sudden death." | ( Gao, J; Jiao, J; Li, PF; Lin, Z; Murtaza, I; Wang, K, 2009) |
| "Cardiac hypertrophy is a risk factor independent of blood pressure; however, the mechanisms that distinguish pathological remodelling due to local cues from pressure overload are unresolved." | ( Desnoyer, R; Karnik, SS; Li, W; Yue, H, 2010) |
| "Cardiac hypertrophy is a common finding in human patients with inborn errors of long-chain fatty acid oxidation." | ( Barnes, S; Cox, KB; Liu, J; Tian, L; Wood, PA; Yang, Q, 2009) |
| "Cardiac hypertrophy is a compensatory enlargement of the heart in response to stress such as hypertension." | ( Anderson, HD; Behbahani, J; Juric, D; Kopilas, MA; Louis, XL; Netticadan, T; Thandapilly, SJ; Wojciechowski, P; Yu, L, 2010) |
| "Cardiac hypertrophy is one of the main ways in which cardiomyocytes respond to mechanical and neurohormonal stimuli." | ( Agrawal, N; Koyani, CN; Rohini, A; Singh, R, 2010) |
| "Cardiac hypertrophy is not only an adaptational state before heart failure but also is an independent risk factor for ischemia, arrhythmia, and sudden death." | ( Hu, D; Li, Y; Liu, N; Ren, L; Sheng, Z; Tang, R, 2010) |
| "Heart hypertrophy is a common cardiac complication of sustained arterial hypertension and is accompanied by an increased incidence of supraventricular tachyarrhythmia, such as atrial fibrillation and atrial flutter." | ( Borlak, J; Zwadlo, C, 2010) |
| "Cardiac hypertrophy is a compensatory enlargement of the heart due to either volume overload (VO) and/or pressure overload (PO) that develops into heart failure if left untreated." | ( Juric, D; Louis, XL; Netticadan, T; Taylor, C; Thandapilly, SJ; Wojciechowski, P; Yu, L, 2010) |
| "Cardiac hypertrophy is one of the most commonly cardiovascular diseases in clinical practice." | ( Chen, C; Fu, Y; Wang, W; Wang, X; Yu, W, 2010) |
| "Cardiac hypertrophy is a major determinant of heart failure." | ( Ai, W; Bai, X; Bian, ZY; Huang, H; Li, H; Liu, C; Tang, QZ; Yan, L; Yin, L; Zhang, Y, 2010) |
| "Cardiac hypertrophy is a major determinant of risk of sudden death and morbidity in HCM." | ( Lombardi, R; Marian, AJ; Nagueh, SF; Tan, Y; Wang, J; Willerson, JT, 2010) |
| "Cardiac hypertrophy is a major risk factor for heart failure and associated patient morbidity and mortality." | ( Arthur, HM; Borthwick, GM; Watkins, SJ, 2011) |
| "Cardiac hypertrophy is characterized by transcriptional reprogramming of fetal gene expression, and histone deacetylases (HDACs) are tightly linked to the regulation of those genes." | ( Cho, YK; Choe, N; Eom, GH; Joung, H; Kee, HJ; Kim, HS; Kim, Y; Ko, JH; Kook, H; Nam, KI; Shin, S, 2011) |
| "Cardiac hypertrophy is another effect of hyperthyroidism, with an increase in the abundance of mitochondria." | ( Atherton, HJ; Clarke, K; Dodd, MS; Griffin, JL; Heather, LC; Radda, GK; Schroeder, MA; Tyler, DJ, 2011) |
| "Cardiac hypertrophy is an adaptive growth process that occurs in response to stress stimulation or injury wherein multiple signal transduction pathways are induced, culminating in transcription factor activation and the reprogramming of gene expression." | ( Aronow, BJ; Elrod, JW; Molkentin, JD; Pu, WT; van Berlo, JH, 2011) |
| "Since pathological cardiac hypertrophy is associated with increased expression of genes involved in glucose handling, this study was undertaken to examine if maternal LP diet alters the expression of genes encoding for some key components of glucose metabolism and uptake, and of the insulin receptor (IR) signal transduction in the heart of male offspring." | ( Aroutiounova, N; Dunn, L; Guzman, C; Tappia, PS, 2013) |
| "Cardiac hypertrophy is controlled by a complex signal transduction and gene regulatory network, containing multiple layers of crosstalk and feedback." | ( Acton, ST; Bass, GT; Dang, ST; Katikapalli, A; Ryall, KA; Saucerman, JJ; Taylor, BE, 2012) |
| "Cardiac hypertrophy is characterised by an imbalance between lipid uptake and fatty acid β-oxidation leading to an accumulation of lipids, particularly triacylglycerol (TAG)." | ( Caldwell, GM; Hauton, D, 2012) |
| "Since cardiac hypertrophy is associated with a substrate switch from fatty acid to glucose, we hypothesized that a reduction in HKII would decrease cardiac hypertrophy after pressure overload." | ( Ardehali, H; Chawla, K; Epting, CL; Ghanefar, M; Laakso, M; Tran, M; Wu, R; Wyatt, E, 2012) |
| "Cardiac hypertrophy is associated with the increase of total amount of RNA, which is in accordance with RNA polymerase II (RNAPII) activation via C-terminal domain (CTD) phosphorylation of the largest subunit of RNAPII." | ( Aonuma, K; Homma, S; Kimura, T; Kuga, K; Maruyama, H; Miyauchi, T; Sakai, S; Shimojo, N; Wang, Z; Yamaguchi, I, 2012) |
| "Cardiac hypertrophy is controlled by a dense signaling network with many pathways associated with cardiac myocyte growth." | ( Ryall, KA; Saucerman, JJ, 2012) |
| "Cardiac hypertrophy is an independent predictor of cardiovascular morbidity and mortality." | ( Guo, WG; Liu, XT; Lu, ZF; Shi, MQ; Su, FF; Wang, HT; Zheng, QS, 2012) |
| "Cardiac hypertrophy is the main response of the heart to various extrinsic and intrinsic stimuli, and it is characterized by specific molecular and phenotypic changes." | ( Anestopoulos, I; Kavo, A; Kortsaris, A; Lazou, A; Panayiotidis, M; Pappa, A; Tentes, I, 2013) |
| "Cardiac hypertrophy is an independent risk factor for sudden cardiac death in clinical settings and the incidence of sudden cardiac death and ventricular arrhythmias are closely related." | ( Chen, B; Chen, F; Chen, M; Dai, M; Ke, J; Tu, J; Wang, X; Xiao, X; Zhang, C, 2012) |
| "Cardiac hypertrophy is an adaptive enlargement of the myocardium in response to altered stress or injury." | ( Wang, J; Yang, X, 2012) |
| "Cardiac hypertrophy is a strong predictor of morbidity and mortality in patients with heart failure." | ( Ferguson, BS; Harrison, BC; Holson, EB; Jeong, MY; McKinsey, TA; Reid, BG; Wagner, FF; Wempe, MF, 2013) |
| "Cardiac hypertrophy is accompanied by significant alterations in energy metabolism." | ( Jaswal, JS; Lopaschuk, GD; Sankaralingam, S; Ussher, JR; Wagg, C; Zaugg, M; Zhang, L, 2013) |
| "Cardiac hypertrophy is an independent predictor of adverse outcomes in patients with heart failure, and thus represents an attractive target for novel therapeutic intervention." | ( Bradner, JE; Cavasin, MA; Demos-Davies, K; McKinsey, TA; Qi, J; Reid, BG; Spiltoir, JI; Stratton, MS, 2013) |
| "Uremic cardiac hypertrophy is associated with activation of the myocardial RAS and the FGFR-1." | ( Bravo, Y; Faul, C; Freundlich, M; Li, YC; Quiroz, Y; Rodriguez-Iturbe, B; Seeherunvong, W; Weisinger, JR, 2014) |
| "Cardiac hypertrophy is associated with a switch towards increased glucose metabolism and decreased fatty acid metabolism." | ( Baines, CP; Douglas, DL; Krenz, M; McCommis, KS, 2013) |
| "Cardiac hypertrophy is a major risk factor for many serious heart diseases." | ( El-Kadi, AO; El-Sherbeni, AA, 2014) |
| "Physiological cardiac hypertrophy is characterized by reversible enlargement of cardiomyocytes and changes in chamber architecture, which increase stroke volume and via augmented convective oxygen transport." | ( Enok, S; Hicks, JW; Slay, CE; Wang, T, 2014) |
| "Cardiac hypertrophy is a complex pathological process that involves multiple factors including inflammation and apoptosis." | ( Chen, K; Chen, Y; Fan, GC; Gao, L; Gong, H; Jiang, DS; Li, H; Liu, PP; Liu, Y; Peng, J; Yang, Q; Zhang, XD; Zhang, XF; Zhang, Y; Zhou, H; Zou, Y, 2014) |
| "Cardiac hypertrophy is a maladaptive change in response to pressure overload, and is also an important risk for developing heart failure." | ( Chen, SL; Iqbal, J; Li, B; Li, MH; Mao, WX; Mi, QY; Wang, ZM; Xie, HG; Yang, SH; Yu, YH; Zhang, YJ, 2014) |
| "Sustained cardiac hypertrophy is often accompanied by maladaptive cardiac remodeling leading to decreased compliance and increased risk for heart failure." | ( Li, PF; Liu, CY; Liu, F; Long, B; Sun, T; Wang, K; Wang, Y; Yuan, SM; Zhang, XJ; Zhou, LY, 2014) |
| "Cardiac hypertrophy is an independent risk factor for cardiovascular disease and its subsequent progression to heart failure represents a major cause of morbidity and mortality in the world." | ( Feng, J; Li, J; Li, P; Li, X; Li, Y; Shen, D; Song, R; Tang, X; Wo, D; Yan, H; Zhang, J, 2014) |
| "Cardiac hypertrophy is controlled by a highly connected signaling network with many effectors of cardiac myocyte size." | ( Bezzerides, VJ; Rosenzweig, A; Ryall, KA; Saucerman, JJ, 2014) |
| "Cardiac hypertrophy is a primary predictor of progressive heart disease that often results in heart failure." | ( Chen, X; Du, W; Gao, X; Ju, J; Li, C; Li, X; Liang, H; Liu, X; Lu, Y; Ma, N; Shan, H; Wang, L; Xu, C; Xu, Z; Yang, B; Zhang, R; Zhang, Y, 2014) |
| "Cardiac hypertrophy is elicited by endothelin (ET)-1 as well as other neurohumoral factors, hemodynamic overload, and oxidative stress; HMG-CoA reductase inhibitors (statins) were shown to inhibit cardiac hypertrophy partly via the anti-oxidative stress." | ( Aonuma, K; Homma, S; Kimura, T; Kuga, K; Maruyama, H; Miyauchi, T; Mizutani, T; Sakai, S; Shimojo, N; Tajiri, K, 2014) |
| "Cardiac hypertrophy is an adaptive reaction of the heart against cardiac overloading, but continuous cardiac hypertrophy is able to induce heart failure." | ( Fan, YY; Li, N; Li, PF; Liu, CY; Liu, F; Long, B; Murtaza, I; Wang, K; Zhou, QY, 2014) |
| "Cardiac hypertrophy is characterized by thickening myocardium and decreasing in heart chamber volume in response to mechanical or pathological stress, but the underlying molecular mechanisms remain to be defined." | ( Cheng, C; Huang, H; Huang, J; Liu, B; Liu, S; Pan, W; Sun, W; Xiong, L; Ye, J; You, X; Zhong, Y, 2014) |
| "Cardiac hypertrophy is a major cause of morbidity and mortality worldwide." | ( Gu, W; Si, L; Wang, F; Wang, X; Xu, J; Xu, X; Yi, C; Zhang, Y, 2014) |
| "As cardiac hypertrophy is a convergence point of risk factors for heart failure, we determined a role for endocannabinoids in attenuating endothelin-1-induced hypertrophy and probed the signaling pathways involved." | ( Akinwumi, BC; Anderson, HD; Lu, Y; Shao, Z, 2014) |
| "A cardiac hypertrophy is defined as an increase in heart mass which may either be beneficial (physiological hypertrophy) or detrimental (pathological hypertrophy)." | ( Bansal, T; Datta, K; Datta, R; Mitra, A; Naskar, S; Pathak, K; Sarkar, S, 2014) |
| "Cardiac hypertrophy is characterized by alterations in both cardiac bioenergetics and insulin sensitivity." | ( Chiong, M; Contreras-Ferrat, A; Gutiérrez, T; Lavandero, S; Lopez-Crisosto, C; Morales, PE; Parra, V; Pennanen, C; Rothermel, BA; Sotomayor-Flores, C; Troncoso, R; Vasquez-Trincado, C, 2014) |
| "Cardiac hypertrophy is a compensatory mechanism that occurs in conjunction with cardiovascular diseases." | ( Gu, J; Guo, Z; Hao, YY; Sun, JM; Wang, AL; Wang, CM; Xie, YJ, 2015) |
| "Cardiac hypertrophy is a major risk factor of cardiovascular morbidity and mortality." | ( Chen, C; Chen, Y; Dong, Y; Liu, C; Tan, W; Wu, D; Wu, L; Xue, R, 2014) |
| "Pathologic cardiac hypertrophy is one of the leading causes of sudden death from cardiac disease and involves a complex network of bio-signaling mechanisms." | ( DaSilva, JN; Fernando, P; Moreau, S; Valdivia, A, 2015) |
| "Cardiac hypertrophy is an adaptive response to pressure, volume stress, and loss of contractile mass from prior infarction." | ( Bu, P; Chen, T; Li, J; Li, N; Liu, H; Liu, J; Wang, S; Zhang, Y, 2015) |
| "Cardiac hypertrophy is a chronic complex disease that occurs in response to hemodynamic load and is accompanied by oxidative stress and mitochondrial dysfunction." | ( de Figueiredo Júnior, IL; Fernandes Facundo, Hd; Gomes Marques de Sousa, TA; Kowaltowski, AJ; Lemos Caldas, FR; Martins, PR; Rocha Leite, IM; Tavarez Filgueiras, AB, 2015) |
| "Cardiac hypertrophy is a key pathophysiological component to biomechanical stress, which has been considered to be an independent and predictive risk factor for adverse cardiovascular events." | ( Chen, Y; Cui, Y; Guo, H; Guo, Y; Shan, T; Wu, D; Xu, D; Zhang, F; Zhang, X; Zhou, H, 2015) |
| "Pathological cardiac hypertrophy is a major predictor for the development of cardiac diseases." | ( Birnbaumer, L; Camacho Londoño, J; Camacho Londoño, JE; Dietrich, A; Flockerzi, V; Freichel, M; Hammer, K; He, T; Kaestner, L; Laufs, U; Lipp, P; Mannebach, S; Mathar, I; Oberhofer, M; Philipp, SE; Reil, JC; Schröder, L; Schweda, F; Tabellion, W; Tian, Q, 2015) |
| "Cardiac hypertrophy is characterized by complex multicellular alterations, such as cardiomyocyte growth, angiogenesis, fibrosis, and inflammation." | ( Akazawa, H; Kamo, T; Komuro, I, 2015) |
| "Cardiac hypertrophy is associated with many forms of heart disease, and identifying important modifier genes involved in the pathogenesis of cardiac hypertrophy could lead to the development of new therapeutic strategies." | ( Bao, D; Dong, W; Liu, N; Lu, D; Lu, YD; Qin, C; Zhang, LF, 2015) |
| "Pathological cardiac hypertrophy is characterized by a shift in metabolic substrate utilization from fatty acids to glucose, but the molecular events underlying the metabolic remodeling remain poorly understood." | ( Cannon, MV; Ciapaite, J; de Boer, RA; de Windt, LJ; Gustafsson, JÅ; Sijbesma, JW; Silljé, HH; Silva, GJ; van der Harst, P; van der Sluis, B; van Deursen, J; van Gilst, WH; Vreeswijk-Baudoin, I, 2015) |
| "Pathological cardiac hypertrophy is characterized by subcellular remodeling of the ventricular myocyte with a reduction in the scaffolding protein caveolin-3 (Cav-3), altered Ca(2+) cycling, increased protein kinase C expression, and hyperactivation of calcineurin/nuclear factor of activated T cell (NFAT) signaling." | ( August, BK; Balijepalli, RC; Hacker, TA; Keefe, AM; Markandeya, YS; Patel, HH; Phelan, LJ; Reynolds, CR; Roth, DM; Woon, MT, 2015) |
| "Cardiac hypertrophy is an abnormal enlargement of heart muscle." | ( Boheler, KR; Huang, Y; Kong, CW; Li, RA; Li, ZC; Poon, E; Wang, Y; Yao, X; Zhang, P, 2015) |
| "Cardiac hypertrophy is accompanied by excessive collagen deposition in the heart." | ( Bansal, T; Chattopadhyay, S; Chawla-Sarkar, M; Datta, K; Datta, R; Rana, S; Sarkar, S, 2015) |
| "Cardiac hypertrophy is a mechanism to compensate for increased cardiac work load, that is, after myocardial infarction or upon pressure overload." | ( Euler, G; Heger, J; Schulz, R, 2016) |
| "Pathological cardiac hypertrophy is regarded as a critical intermediate step toward the development of heart failure." | ( Cartwright, EJ; Chowdhury, SK; Lei, M; Liang, Q; Liu, W; Prehar, S; Tsui, H; Wang, S; Wang, X; Zi, M, 2015) |
| "Cardiac hypertrophy is an important risk factor for heart failure." | ( Li, X; Liang, G; Liu, Z; Peng, K; Qian, Y; Skibba, M; Tian, X; Wang, J; Xu, Z; Zou, C, 2016) |
| "Cardiac hypertrophy is a key pathological process of many cardiac diseases." | ( An, X; Bai, Y; Li, H; Lu, Z; Song, Y; Wang, J; Xiao, H; Zhang, Y, 2016) |
| "Cardiac hypertrophy is a major risk factor for heart failure." | ( Cantarella, D; Cimino, J; Comoglio, PM; Crepaldi, T; Fontani, L; Gallo, S; Gatti, S; Medico, E; Morello, M; Natale, M; Ponzetto, A; Sala, V; Vigna, E, 2016) |
| "Cardiac hypertrophy is associated with growth and functional changes of cardiomyocytes, including mitochondrial alterations, but the latter are still poorly understood." | ( Bloks, VW; de Boer, RA; de Jong, AM; Silljé, HH; Tigchelaar, W; van Gilst, WH, 2016) |
| "Pathological cardiac hypertrophy is a maladaptive response in a variety of organic heart disease (OHD), which is characterized by mitochondrial dysfunction that results from disturbed energy metabolism." | ( Chen, S; Ding, Y; He, P; Jiang, J; Li, Z; Liu, P; Lu, X; Ma, Y; You, J; Yue, Z, 2016) |
| "Cardiac hypertrophy is the greatest complication in metabolic syndrome (MS), in dams and in offspring." | ( Carreras, O; Murillo, ML; Nogales, F; Ojeda, ML; Serrano, A; Sobrino, P, 2016) |
| "Pathological cardiac hypertrophy is associated with nearly all forms of heart failure." | ( Han, X; Ma, B; Zhou, L, 2016) |
| "Cardiac hypertrophy is one of the major risk factors of cardiovascular morbidity and mortality." | ( Chen, C; Chen, Y; Dong, B; Dong, Y; Liu, C; Sun, Y; Tan, W; Xue, R; Zeng, J; Zhao, J, 2017) |
| "Cardiac hypertrophy is a complex process involving highly coordinated but tight regulation of multiple elements, such as in epigenetics, which make an important contribution to myocardium remodeling and cardiac hypertrophy." | ( Li, S; Luo, X; Peng, C; Sun, H, 2017) |
| "Cardiac hypertrophy is associated with autonomic imbalance, characterized by enhanced sympathetic activity and withdrawal of parasympathetic control." | ( Chen, LN; He, X; Liu, JJ; Liu, LZ; Lu, Y; Sun, L; Yu, XJ; Zang, WJ; Zhao, M, 2017) |
| "Cardiac hypertrophy is a critical component of phenotype in the failing heart." | ( Chen, G; Hu, L; Jiang, R; Lin, C; Ping, J; Shan, J; Shao, M; Tian, H; Wang, L; Zhuo, C, 2017) |
| "Cardiac hypertrophy is a thickening of the heart muscle that is associated with cardiovascular diseases such as hypertension and myocardial infarction." | ( Fan, Z; Luo, X; Lv, N; Tan, W, 2017) |
| "Cardiac hypertrophy is characterized by increased myofibrillogenesis." | ( Chen, J; Chen, XM; Hou, JW; Li, G; Li, W; Li, YG; Wang, H; Wang, Q; Wang, YP; Wei, SS; Xu, WP; Zhou, Q, 2017) |
| "Cardiac hypertrophy is a crucial predictor of heart failure and is regulated by microRNAs." | ( Bao, Q; Chen, L; Li, J; Liu, X; Wu, S; Wu, W; Zhao, M, 2017) |
| "Cardiac hypertrophy is an adaptive response triggered by many physiological and pathological conditions and will lead to heart failure eventually." | ( Dong, B; Dong, Y; Liu, C; Sun, Y; Xue, R, 2017) |
| "Hypertensive cardiac hypertrophy is associated with reduced coronary flow reserve, but its impact on coronary flow regulation and vasomotor function remains incompletely understood and requires further investigation." | ( Hein, TW; Kuo, L; Lu, G; Ren, Y; Tsai, SH; Xu, X, 2017) |
| "Cardiac hypertrophy is a compensatory mechanism maladapted because it presents an increase in the oxidative stress which could be associated with the development of the heart failure." | ( Altamirano, J; García, N; González-Mondellini, FA; Pérez-Treviño, P; Rivera-Álvarez, I; Vela-Guajardo, JE, 2017) |
| "Cardiac hypertrophy is closely linked to impaired fatty acid oxidation, but the molecular basis of this link is unclear." | ( Berman, AG; Damen, FW; Ellis, JM; Goergen, CJ; Harris, KL; Hasek, LY; Pereyra, AS, 2017) |
| "Cardiac hypertrophy is the risk factor of heart failure when the heart is confronted with pressure overload or neurohumoral stimuli." | ( Chen, Y; Dong, B; Dong, Y; Jiang, J; Liu, C; Sun, Y; Tan, W; Xue, R; Zhao, J, 2017) |
| "The development of cardiac hypertrophy is a complicated process, which undergoes a transition from compensatory hypertrophy to heart failure, and the identification of new biomarkers and targets for this disease is greatly needed." | ( Pistolozzi, M; Shi, X; Su, H; Sun, X; Tan, W, 2017) |
| "Cardiac hypertrophy is an adaptive response triggered by pathological stimuli." | ( Chiong, M; Eura, Y; Garrido, V; Kokame, K; Lavandero, S; Navarro-Marquez, M; Pedrozo, Z; Roa, JC; Romero, D; Torrealba, N; Villalobos, E, 2017) |
| "Cardiac hypertrophy is determined by an increase of cell size in cardiomyocytes (CMCs)." | ( Ceci, M; Gallo, P; Ricciardi, S; Romano, N, 2018) |
| "Cardiac hypertrophy is a major characteristic of early-stage hypertension-related heart failure." | ( Chen, RJ; Ho, TJ; Huang, CY; Kuo, CH; Kuo, WW; Lin, YM; Pai, PY; Tsai, FJ; Vijaya Padma, V, 2018) |
| "Pathological cardiac hypertrophy is the main determinant of the development of heart failure, for which there is often no effective therapy." | ( Gong, H; Lian, X; Peng, F; Wang, L; Ye, N; Zhang, H, 2018) |
| "Cardiac hypertrophy is one of the initial symptoms of many heart diseases." | ( Lu, Y; Wu, F, 2018) |
| "Cardiac hypertrophy is a common consequence of chronic hypertension and leads to heart failure and premature death." | ( Amaral, JH; Castro, MM; Dos Passos, MA; Gerlach, RF; Guimaraes, DA; Pinheiro, LC; Rizzi, E; Tanus-Santos, JE, 2018) |
| "Pathological cardiac hypertrophy is associated with the accumulation of lipid peroxidation-derived aldehydes such as 4-hydroxy-trans-2-nonenal (HNE) and acrolein in the heart." | ( Baba, SP; Bhatnagar, A; Brittian, KR; Conklin, DJ; Dassanayaka, S; Jagatheesan, G; Jones, SP; Merchant, ML; Schmidtke, VK; Singh, M; Xie, Z; Zhang, D; Zhao, J, 2018) |
| "Cardiac hypertrophy is one of the key structural changes in diabetic cardiomyopathy." | ( Ding, S; Huang, B; Huang, J; Jiang, Q; Qiu, H; Wu, Q; Zhang, J, 2018) |
| "Cardiac hypertrophy is one of the major risk factors for chronic heart failure." | ( Liu, HQ; Liu, Y; Luo, JD; Shen, HJ; Wang, XQ; Zheng, LY, 2018) |
| "Cardiac hypertrophy is a common response of cardiac myocytes to stress and a predictor of heart failure." | ( Frank, DU; Saucerman, JJ; Sutcliffe, MD, 2018) |
| "Cardiac hypertrophy is associated with mitochondrial dysfunctions, which leads to heart failure if sustained." | ( Guven, C, 2018) |
| "Cardiac hypertrophy is commonly involved in cardiac injury." | ( Cheng, JT; Cheng, KC; Cheng, YZ; Kuo, SC; Lee, WJ; Li, Y, 2018) |
| "Pathological cardiac hypertrophy is the main risk factor for heart diseases." | ( Bi, HL; Lai, S; Li, HH; Shu, Q; Wang, XM; Yang, XL; Zhang, YL, 2018) |
| "Cardiac hypertrophy is a pathophysiological response to various pathological stresses and ultimately leads to heart failure." | ( Dai, G; Dong, B; Dong, Y; Fan, W; Huang, H; Jiang, J; Liang, Z; Liu, C; Su, Q; Sun, Y; Wang, Y; Xue, R; Zhao, J, 2018) |
| "Cardiac hypertrophy is a maladaptive response to pressure overload and it's an important risk factor for heart failure and other adverse cardiovascular events." | ( Chen, X; Cui, S; Cui, Y; Ding, S; Guo, H; Li, Y; Qin, W; Wang, H; Wu, D; Zhang, Y, 2018) |
| "Cardiac hypertrophy is characterized by myocyte hypertrophy, accumulation of cardiac collagen, and reactivation of fetal genes." | ( Kong, CY; Liu, YL; Song, P; Tang, QZ; Zhao, XS; Zhou, H, 2018) |
| "Sustained cardiac hypertrophy is a major cause of heart failure (HF) and death." | ( Bi, HL; Chen, C; Li, HH; Lin, QY; Wang, QS; Wang, S; Xie, X; Yan, X; Zhang, YL; Zou, LX, 2019) |
| "Cardiac hypertrophy is a major predisposing factor for heart failure and sudden cardiac death." | ( Chen, N; Gao, L; Li, L; Liu, Y; Wang, X; Xiao, L; Yang, L; Zhang, J; Zhao, X, 2018) |
| "Cardiac hypertrophy is related to oxidative stress-induced damage." | ( Cao, D; Dai, J; Ji, G; Liu, Y; Nyirimigabo, E; Wang, H; Wang, J; Wang, Z; Wei, B; Zhang, M; Zhang, X, 2019) |
| "Cardiac hypertrophy are the major health challenges in the whole world." | ( An, X; Lang, P; Wang, F; Xie, Y; Zhang, N, 2019) |
| "Cardiac hypertrophy is a key pathological process in the context of diabetic cardiomyopathy." | ( Ding, S; Huang, B; Huang, J; Jiang, Q; Qiu, H; Zhang, J; Zhou, P, 2019) |
| "Cardiac hypertrophy is a risk factor which can intrigue heart failure." | ( Hu, X; Li, T; Liu, J; Ou-Yang, Q; Wang, L; Xie, X, 2019) |
| "Although cardiac hypertrophy is widely recognized as a risk factor that leads to cardiac dysfunction and, ultimately, heart failure, the complex mechanisms underlying cardiac hypertrophy remain incompletely characterized." | ( Dai, FF; Fu, ZF; Mei, YW; Wang, H; Xue, L; Yang, MH; Yin, Z; Zang, MX; Zhang, S; Zhang, SF; Zhou, MJ, 2019) |
| "Cardiac hypertrophy is a common pathological change frequently accompanied by chronic hypertension and myocardial infarction." | ( Ba, L; Cao, Y; E, M; Fu, B; Qi, H; Ren, J; Shi, P; Song, C; Sun, H; Zhang, Q, 2019) |
| "Cardiac hypertrophy is a myocardial enlargement due to overload pressure, and the primary cause of heart failure." | ( Chen, P; Deng, Y; Feng, H; Huang, L; Ouyang, W; Wang, J; Wu, J; Xian, J; Zhu, G, 2019) |
| "Cardiac hypertrophy is a one of common type of CHD, responsible for cardiac mortality worldwide." | ( Peng, L; Yan, K; Zhang, H; Zheng, N; Zhou, K, 2018) |
| "Cardiac hypertrophy is widely diagnosed in clinical cardiac disorders." | ( Chang, WT; Chen, ZC; Cheng, JT; Cheng, KC; Li, Y; Tsai, CC, 2019) |
| "Cardiac hypertrophy is an important risk factor for heart failure." | ( Hwang, KC; Kim, SW; Lee, CY; Lee, J; Lee, S; Lim, S; Seo, HH; Shin, S, 2019) |
| "Cardiac hypertrophy is the main cause of heart failure and sudden death in patients." | ( Chen, H; He, J; Jiang, W; Lan, J; Li, H; Li, R; Li, X; Tang, CS; Wang, X; Wu, S; Wu, Y; Xin, J; Xue, K; Zhuo, C, 2019) |
| "Thus, pathological cardiac hypertrophy is a major risk factor for many cardiovascular diseases and death in humans." | ( Li, P; Wang, K; Yan, K, 2019) |
| "Cardiac hypertrophy is a common pathological change found in various cardiovascular diseases." | ( Bi, X; Hong, H; Lu, J; Wang, J; Ye, J; Yu, Y; Yuan, J; Zhang, Y, 2019) |
| "Cardiac hypertrophy is an adaptive response of the myocardium to pressure or volume overload." | ( Ba, L; Cao, Y; Chen, Y; Dong, C; Gao, J; Guan, X; Pan, H; Qi, H; Shi, P; Song, C; Sun, H; Zhang, Q, 2019) |
| "Cardiac hypertrophy is a result of cardiac response to excessive heart burden." | ( Jing, L; Li, S; Wang, J; Zhang, G, 2019) |
| "Thus, cardiac hypertrophy is uncoupled from profibrotic signaling in this mouse model, which we tie to a requirement for the LINC complex in productive TGFβ signaling." | ( King, MC; Rodriguez, EC; Stewart, RM, 2019) |
| "Cardiac hypertrophy is a compensatory response in reaction to mechanical load that reduces wall stress by increasing wall thickness." | ( Chen, X; Cui, Y; Du, B; Fan, C; Guo, H; Li, Y; Wang, H; Wu, D; Yang, H; Zhai, Q; Zhang, J; Zhou, H, 2019) |
| "Considering that cardiac hypertrophy is commonly associated to hyperthyroidism condition, the present study aimed to investigate the contribution of UPS in cardiac hypertrophy induced by thyroid hormones." | ( Barreto-Chaves, ML; Demasi, M; Lino, CA, 2019) |
| "Cardiac hypertrophy is an adaptive response to abnormal physiological and pathological stimuli, which can be classified into concentric and eccentric hypertrophy, induced by pressure overload or volume overload, respectively." | ( Dai, F; Li, C; Wu, J; Zou, Y, 2020) |
| "Cardiac hypertrophy is considered to be a leading factor in heart function-related deaths." | ( Cao, Y; Chen, J; Gu, B; Gu, S; Jin, Y; Jin, Z; Li, X; Li, Y; Ma, L; Ning, Z; Tian, J; Tu, J; Wang, Z, 2020) |
| "At initial stages, cardiac hypertrophy is associated with normal or enhanced cardiac function and is considered to be adaptive or physiological; however, at later stages, if the stimulus is not removed, it is associated with contractile dysfunction and is termed as pathological cardiac hypertrophy." | ( Dhalla, NS; Duhamel, TA; Oldfield, CJ, 2020) |
| "Cardiac hypertrophy is an independent predictor of CVD." | ( Che, C; Dudick, K; Shoemaker, R, 2019) |
| "Cardiac hypertrophy is a heart reaction to the increase of cardiac load, with the characteristics of increased expression of cardiac hypertrophy markers, enhanced protein synthesis, and enlarged cell area." | ( Li, Q; Wang, F; Wei, X; Zhang, J; Zhang, W, 2020) |
| "Cardiac hypertrophy is an early milestone of many heart diseases." | ( Liang, C; Luo, Y; Xu, Y; Zhang, T, 2020) |
| "Pathological cardiac hypertrophy is a classical hallmark of heart failure." | ( Angermann, JE; Bender, A; Burnett, L; Evans, LW; Ferguson, BS; Godoy, L; Shen, Y; Staten, D; Zhou, T, 2020) |
| "Cardiac hypertrophy is a prominent feature of heart remodeling, which may eventually lead to heart failure." | ( Baruscotti, M; Guo, R; Liu, H; Liu, N; Wang, Y; Zhang, H; Zhang, J; Zhao, L, 2020) |
| "Cardiac hypertrophy is a key pathologic process in heart failure." | ( Fan, D; Pan, W; Qi, J; Tan, Y; Wu, J; Xu, W; Yu, J; Zhang, M, 2020) |
| "Pathological cardiac hypertrophy is characterized by myocyte enlargement and cardiac dysfunction." | ( Chen, W; Wang, Y; Zhang, Y, 2020) |
| "Pathological cardiac hypertrophy is a major risk factor for cardiovascular morbidity and mortality." | ( Jiang, C; Lu, Y; Zhang, S, 2020) |
| "Cardiac hypertrophy is an adaptive response to manage an excessive cardiac workload and maintain normal cardiac function." | ( Conejeros, C; Olmedo, I; Parra, V; Pedrozo, Z; Sanchez, G, 2020) |
| "Cardiac hypertrophy is one of most important risk factors for cardiovascular mortality." | ( Jiang, W; Lei, L; Li, Q; Ni, Y; Wan, Z; Wei, J, 2020) |
| "Cardiac hypertrophy is an independent risk factor of many cardiovascular diseases." | ( Abdel-Kader, MS; Albaqami, FF; Alharthy, KM; Althurwi, HN; Salkini, MA, 2020) |
| "Pathological cardiac hypertrophy is ultimately accompanied by cardiomyocyte apoptosis." | ( Hu, J; Li, W; Lin, S; Lyu, Q; Wu, G; Yang, J; Yang, Q, 2020) |
| "Cardiac hypertrophy is an adaptive response to stress, in order to maintain proper cardiac function." | ( Bhadra, MP; Bhukya, CK; Chakrabarti, M; Manchineela, S; Mendonza, JJ; Naini, R; Nallari, P; Raut, GK; Reddy, VD; Suresh, Y; Venkateshwari, A, 2020) |
| "Cardiac hypertrophy is a common pathological condition and an independent risk factor that triggers cardiovascular morbidity." | ( Bai, L; Chen, L; Fan, Y; Gan, M; Guo, Z; Hao, X; Jiang, D; Li, X; Shen, L; Tan, Y; Zhang, S; Zhu, L, 2020) |
| "Cardiac hypertrophy is the underlying cause of heart failure and is characterized by excessive oxidative stress leading to collagen deposition." | ( Chakrapani, LN; Kalaiselvi, P; Kishore Kumar, SN; Mohan, T; Ravi, DB; Singh, A; Srinivasan, A; Varadharaj, S; Velusamy, P, 2020) |
| "Cardiac hypertrophy is a well-known major risk factor for poor prognosis in patients with cardiovascular diseases." | ( Fujii, S; Kajii, T; Kato, T; Kobayashi, S; Kohno, M; Mizukami, Y; Nakamura, Y; Oda, T; Okuda, S; Uchinoumi, H; Watanabe, K; Yamamoto, T; Yano, M; Yoshitomi, R, 2020) |
| "Cardiac hypertrophy is a major risk factor for heart failure and leads to cardiovascular morbidity and mortality." | ( Han, BH; Kang, DG; Kim, HY; Lee, HS; Lee, YJ; Son, CO; Yoon, JJ, 2020) |
| "Pathological cardiac hypertrophy is associated with many diseases including hypertension." | ( Chen, RJ; Ho, TJ; Huang, CY; Kumar, VB; Kuo, CH; Lin, KH; Padma, VV; Shanmugam, T; Shibu, MA; Yeh, YL, 2021) |
| "Cardiac hypertrophy is an important prepathology of, and will ultimately lead to, heart failure." | ( Cao, S; Chen, F; Chen, H; Da, Q; Gao, Y; Han, Y; Hu, L; Huang, Z; Ji, Y; Li, C; Miao, Q; Shao, Y; Shi, Z; Sun, S; Wang, L; Wei, Y; Wu, L; Wu, W; Xie, L; Yan, K; Zhang, Y, 2021) |
| "Pathological cardiac hypertrophy is the leading cause of heart failure, and miRNAs have been recognized as key factors in cardiac hypertrophy." | ( Chen, C; Lu, Q; Shi, JY; Su, YL; Xu, X, 2021) |
| "Cardiac hypertrophy is a current, major, global health challenge." | ( Chu, Z; Han, B; Han, J; Lu, Q; Shi, X; Zhang, B; Zhang, X, 2021) |
| "Pathological cardiac hypertrophy is a common cause of heart failure." | ( Chen, H; Gao, Z; Gong, M; Li, C; Li, K; Meng, Y; Wang, L; Zhang, H; Zhang, X; Zheng, C; Zheng, Y, 2022) |
| "Cardiac hypertrophy is one of the initial disorders of the cardiovascular system and can induce heart failure." | ( Chu, Z; Han, B; Han, J; Huang, P; Shi, X; Zhang, B; Zhang, X, 2021) |
| "Cardiac hypertrophy is the early stage of many heart diseases, such as coronary heart disease, hypertension, valvular dysfunction and cardiomyopathy." | ( Fan, W; Hu, Z; Wu, C; Wu, H; Wu, J; Wu, S; Wu, X; Yang, L; Yang, X; Zhang, B; Zhang, J, 2021) |
| "Cardiac hypertrophy is an adaptive response of the myocardium to pressure overload or adrenergic agonists." | ( Bai, L; Han, X; Jeong, MH; Kee, HJ; Kee, SJ; Zhao, T, 2021) |
| "Cardiac hypertrophy is a compensatory response to pressure overload, which eventually leads to heart failure." | ( Feng, J; Gong, J; Lin, X; Liu, J; Ma, S; Nie, S; Tang, Y; Wang, L, 2021) |
| "Cardiac hypertrophy is a pivotal pathophysiological step of various cardiovascular diseases, which eventually leads to heart failure and death." | ( Baruscotti, M; Chang, Y; Difrancesco, D; Kang, Y; Shang, Y; Wang, Y; Xu, L; Yu, M; Zhang, S; Zhao, H; Zhao, L; Zhao, X, 2022) |
| "Pathological cardiac hypertrophy is a characteristic feature in many cardiovascular diseases (CVDs)." | ( Kulhari, U; Kumar, A; Kundu, S; Mugale, MN; Murty, US; Ram, C; Sahu, BD; Syed, AM, 2022) |
| "Cardiac hypertrophy is a complex process induced by the activation of multiple signaling pathways." | ( Han, X; Luo, X; Mao, Q; Peng, B; Peng, C; Wu, S; Zhang, H, 2021) |
| "Cardiac hypertrophy is a key structural change in diabetic cardiomyopathy, which mechanism is unknown." | ( Ding, S; Jiang, C; Jiang, Q; Qiu, H; Wu, K; Yang, C; Yang, J; Zhang, J, 2022) |
| "Cardiac hypertrophy is a leading cause of cardiac morbidity and mortality worldwide." | ( Chen, L; Chen, W; Huang, S; Li, L; Mao, H; Ouyang, X; Yang, Y; Zhang, K, 2022) |
| "Cardiac hypertrophy is a major risk factor for developing heart failure." | ( Cui, YK; Han, WM; Hong, YX; Li, GR; Wang, Y; Wu, C; Wu, WY; Wu, Y, 2022) |
| "Cardiac hypertrophy is one of the most common risk factors for heart failure." | ( Duan, J; Li, T; Liang, Q; Lin, L; Ma, Y; Sun, M; Sun, Z; Wang, F, 2022) |
| "Pathological cardiac hypertrophy is the most important risk factor for developing chronic heart failure." | ( Cai, WJ; Chen, M; Dai, Y; Fan, CL; Guo, J; Hou, YL; Liang, S; Ye, MN, 2022) |
| "Cardiac hypertrophy is an adaptive and compensatory mechanism preserving cardiac output during detrimental stimuli." | ( Cheng, Z; Feng, J; Gao, Y; Hou, L; Li, C; Wang, J; Zhou, J, 2022) |
| "Cardiac hypertrophy is a leading risk for heart failure and sudden death." | ( Ji, H; Peng, W; Qu, J; Yang, L, 2022) |
| "Pathological cardiac hypertrophy is an independent risk factor for heart failure and is considered a target for the treatment of heart failure." | ( Gao, Y; Guo, X; Hu, L; Li, Y; Liu, Y; Ma, S; Tang, J; Wang, Z; Wei, J; Zhang, Q; Zhang, X; Zhang, Y, 2022) |
| "Pathological cardiac hypertrophy is an independent risk factor of cardiovascular diseases." | ( Ding, YY; Hong, JH; Li, JM; Liu, Y; Pan, XC; Zhang, HG, 2022) |
| "Cardiac hypertrophy is initially an adaptive response of cardiomyocytes to neurohumoral or hemodynamic stimuli." | ( Dai, S; Fan, X; Han, B; Han, J; Hong, X; Huang, W; Lin, S; Lin, W; Shi, X; Su, L; Xu, J; Ye, B; Zhong, L; Zhong, X, 2022) |
| "Cardiac hypertrophy is a feature of hypertrophic cardiomyopathy (HCM), which could lead to heart failure and other cardiovascular diseases." | ( Chen, J; Huang, N; Li, J; Sun, X; Wang, X; Zeng, Z; Zhang, H; Zou, Z, 2022) |
| "Cardiac hypertrophy is a crucial preliminary step in heart failure, but its treatment has not yet been fully successful." | ( Akiba, Y; Fukuda, K; Funahashi, A; Hashimoto, H; Katsuki, T; Kimura, M; Komuro, J; Kuoka, T; Kusumoto, D; Nakamura, T; Seki, T; Tokuoka, Y; Yamada, T; Yuasa, S, 2022) |
| "Cardiac hypertrophy is necessary for the heart to accommodate an increase in workload." | ( Alharbi, HO; Clerk, A; Cooper, STE; Cull, JJ; Fuller, SJ; Glennon, PE; Hardyman, MA; Markou, T; Sugden, PH, 2022) |
| "Cardiac hypertrophy is a crucial risk factor for hypertensive disorders during pregnancy, but its progression during pregnancy remains unclear." | ( Fukamizu, A; Kim, JD; Kwon, C; Mori, H; Muroi, SI; Muromachi, N; Nakagawa, Y; Nakamura, K; Saito, H; Yamada, Y, 2023) |
| "Cardiac hypertrophy is a well-established risk factor for cardiovascular mortality worldwide." | ( Dong, Z; Li, T; Lu, J; Sheng, S; Shi, Y; Yuan, M; Yue, L, 2023) |
| "Pathological cardiac hypertrophy is one of the main activators of heart failure." | ( Chang, J; Dong, Z; Fan, C; Jiao, Y; Jin, Q; Li, X; Que, Y; Song, Q; Yang, C; Zhang, Y, 2023) |
| "Cardiac hypertrophy is accompanied by increased myocardial oxidative stress, and whether naringenin, a natural antioxidant, is effective in the therapy of cardiac hypertrophy remains unknown." | ( He, B; He, Y; Li, Y; Xia, T; Zeng, C; Zhang, C, 2023) |
| "Pathological cardiac hypertrophy is a major cause of heart failure, and there is no effective approach for its prevention or treatment." | ( Deng, H; Jiang, Z; Liu, H; Liu, X; Ren, Z; Tian, Z; Wu, Z; Zhou, Z, 2023) |
| "Cardiac hypertrophy is associated with increased translation." | ( Harris, M; Kennedy, LM; Murphy, E; Rodriguez, R, 2023) |
| "Cardiac hypertrophy is associated with diastolic heart failure (DHF), a syndrome in which systolic function is preserved but cardiac filling dynamics are depressed." | ( Betancourt, L; Cazorla, O; de Tombe, PP; Dewan, S; Kumar, M; Mayer, BJ; Witayavanitkul, N, 2023) |
| "Cardiac hypertrophy is the heart's compensatory response stimulated by various pathophysiological factors." | ( Jia, B; Jia, S; Leng, M; Liu, R; Weng, L; Xiong, Y; Yan, S; Yang, F; Ye, J; Zhao, J; Zheng, M; Zhou, Y, 2023) |
| "Cardiac hypertrophy is a common structural remodeling in many cardiovascular diseases." | ( Hou, Y; Ji, W; Li, L; Li, T; Li, X; Li, Y; Liang, H; Lv, L; Shan, H; Yang, N; Yang, R; Yu, T; Zhang, J; Zhang, Y, 2023) |
| "Pathological cardiac hypertrophy is associated with ventricular fibrosis leading to heart failure." | ( Bandyopadhyay, A; Banik, A; Datta Chaudhuri, R; Gupta, S; Kar, A; Kundu, B; Sarkar, S; Vashishtha, S, 2023) |
| "Pathological cardiac hypertrophy is one of the most significant phenotypes of HF." | ( Han, L; Huang, K; Li, Q; Wu, H; Wu, L; Xu, X, 2023) |
| "Pathological cardiac hypertrophy is a hallmark of various cardiovascular diseases (CVD) including chronic heart failure (HF) and an important target for the treatment of these diseases." | ( Chen, J; Ma, E; Peng, L; Ren, DN; Wo, D; Wu, C; Yan, H; Zhu, W, 2023) |
| "Cardiac hypertrophy is frequently associated with ventricular dysfunction and heart failure." | ( Ding, L; Dong, H; Jia, W; Lin, S; Lin, Y; Ren, S; Wang, Y; Wei, C; Xiao, D; Yan, P; Zhang, Y; Zhao, Y, 2023) |
| "Cardiac hypertrophy is an adaptive response to various pathological insults, including hypertension." | ( Cho, S; Jeong, D; Lee, C, 2023) |
| "Cardiac hypertrophy is studied in relation to energy metabolism, autophagy, and ferroptosis, which are associated with cardiovascular adverse events and chronic heart failure." | ( Geng, J; Lv, C; Meng, Y; Yuan, H; Zhou, L, 2024) |
| Excerpt | Reference |
|---|
| "Severe cardiac hypertrophy has been produced experimentally in rats by long-term, low-dose treatment with tri-iodothyroacetic acid." | ( Hawkey, CM; Olsen, EG; Symons, C, 1975) |
| "The effect of manidipine on cardiac hypertrophy, coronary circulation, left ventricular weight and maximal coronary flow in hypertension was measured in DOCA/salt treated systolic hypertensive rats with and without manidipine treatment." | ( Asayama, J; Itoh, H; Kuwabara, T; Nakagawa, M; Nakata, T; Sasaki, S; Takeda, K; Takesako, T; Tanabe, S; Yamahara, Y, 1992) |
| "Two experimental models of cardiac hypertrophy (chronic thyroxine or isoprenaline treatment of adult rats) were compared 24 h and five weeks after the agent was last given." | ( Cihák, R; Kolár, F; Ostádal, B; Pelouch, V; Procházka, J; Widimský, J, 1992) |
| "Concomitantly, cardiac hypertrophy was attenuated in the treated group compared with the placebo group (heart-to-body weight ratios of 4." | ( Nayler, WG, 1991) |
| "Therefore, hypertension and cardiac hypertrophy were dissociable in this model when pindolol was administered from the onset of hypertension." | ( Cimini, CM; Gonzalez, MA; Weiss, HR, 1991) |
| "At the end of treatment, cardiac hypertrophy, coronary vascular reserve, density and cross-sectional surface area of the myocardial capillaries (normalized for the myocardial mass) and wall/lumen ratio of the coronary arterioles were determined." | ( Clozel, JP; Hefti, F; Kuhn, H, 1989) |
| "To investigate the relationship between cardiac hypertrophy associated with hypertension, and the alterations in myocardial lipid metabolism, nicardipine (160 mg/kg/day), hydralazine (40 mg/kg/day), and enalapril (30 mg/kg/day) were administered to spontaneously hypertensive rats from 20 to 24 weeks of age." | ( Fujii, S; Kawaguchi, H; Okamoto, H; Saito, H; Togashi, H; Yasuda, H, 1988) |
| "Regression of cardiac hypertrophy is possible by differentiated pharmacotherapy, e." | ( Strauer, BE, 1985) |
| "Reversal of cardiac hypertrophy has been obtained by treatment with some antihypertensive drugs but has not been achieved consistently with beta blockers." | ( Almeida, JB; Amorin, MP; Bessa, AM; Cezaretti, ML; Ramos, OL; Saragoça, MA; Tavares, A, 1988) |
| "In order to investigate the role of cardiac hypertrophy in atrial natriuretic peptide (ANP) secretion in patients with essential hypertension, plasma levels of ANP were measured after overnight rest in 36 patients with untreated hypertension and in 31 normotensive controls." | ( Bönner, G; Kaufmann, W; Stimpel, M; Wambach, G, 1988) |
| "Isoprenaline treatment causes cardiac hypertrophy and an accumulation of N1-acetylspermidine in the rat heart." | ( Garber, PM; Mezl, VA; Rakusan, K; Villemure, C, 1988) |
| "Regression of cardiac hypertrophy has been proven to occur in experimental animals following some types of antihypertensive therapy." | ( Sen, S, 1983) |
| "Marked cardiac hypertrophy, as indicated by increase heart weight and increased size of cardiac muscle cells, was evidenced in iron-deficient rats, while the heart weights and myocardial cell size of drug-treated anaemic rats were in the normal range." | ( Carillo, SV; Rossi, MA, 1982) |
| "Development of cardiac hypertrophy and increases in systolic and diastolic blood pressure were dependent upon prolonged periods of thyroid-treatment lasting from 3 days to 4 weeks, whereas the maximal increase (about 55%) in heart rate was seen after the first week of thyroid-treatment." | ( Sakanashi, M; Takeo, S; Tomomatsu, E, 1984) |
| "At 25 weeks of age, cardiac hypertrophy was noted to the same extent in either treated group." | ( Hirata, M; Imamoto, T; Shimamoto, N; Tanabe, M, 1982) |
| "However, cardiac hypertrophy as measured by the increase in cardiac mass was not prevented by such treatment with 1,3-diaminopropanol, showing that the increased content of polyamines was not essential for the hypertrophic response." | ( Hibasami, H; Pegg, AE, 1980) |
| "Regression of cardiac hypertrophy, however, was seen only in the alpha-methyldopa-treated group, as judged by changes in left ventricular weight, RNA/DNA ratio, and hydroxyproline content." | ( Limas, CJ; Spier, SS, 1980) |
| "Thus, reversal of cardiac hypertrophy with antihypertensive treatment is possible in human beings; however, it seems to depend on other factors besides blood pressure control." | ( Fouad, FM; Nakashima, Y; Salcedo, EE; Tarazi, RC, 1982) |
| "In MCTP-treated rats, right heart hypertrophy was observed at 11 days and became more pronounced at 14 days." | ( Roth, RA; Schultze, AE, 1993) |
| "Regression of cardiac hypertrophy occurred after treatment of aortic banded rats with a high dose of enalapril, bunazosin or propranolol, and was accompanied by a reduction in systolic blood pressure." | ( Hata, T; Makino, N; Matsui, H; Nakanishi, H; Yanaga, T; Yano, K, 1994) |
| "A clear trend towards a reduction of cardiac hypertrophy during the treatment is suggested by the significant decrements of the indices measured." | ( Genovesi-Ebert, A; Ghione, S; Marabotti, C; Noseda, A; Spinazzi, A, 1994) |
| "Both treatments significantly reduced cardiac hypertrophy, but alatriopril showed a greater efficacy than captopril--the increase in relative heart weight reaching 38% with captopril and only 22% with alatriopril (P < ." | ( Bralet, J; Gros, C; Lecomte, JM; Marie, C; Mossiat, C; Schwartz, JC, 1994) |
| "We investigated the effect on cardiac hypertrophy of a once-daily treatment with lacidipine, at doses that do not reduce systolic blood pressure." | ( Accordini, C; Cristofori, P; Micheli, D; Sbarbati, A; Terron, A, 1994) |
| "The prevention of cardiac hypertrophy was most marked in the SHRSP treated with perindopril plus N(G)-nitro-L-arginine methyl ester, despite blood pressure being higher in this group than in the two other treatment groups." | ( Anderson, NH; Bohr, DF; Devlin, AM; Dominiczak, AF; Lee, WK; Reid, JL, 1996) |
| "This treatment induced cardiac hypertrophy with increases in heart rate and systolic blood pressure." | ( Hakamata, N; Hamada, H; Nakamura, H; Ohsuzu, F, 1997) |
| "We have studied the induction of cardiac hypertrophy after treatment with clenbuterol and the role of polyamines in this effect." | ( Balaña-Fouce, R; Cubría, JC; Ordóñez, C; Ordóñez, D; Reguera, R, 1998) |
| "SHR-S exhibited a small degree of cardiac hypertrophy (LV/BW was 8% higher than in WKY but 11% less than in untreated SHR), but LV/BW was normalized in SHR-L (to within 1% of WKY LV/BW)." | ( Head, GA; Thomas, CJ; Woods, RL, 1998) |
| "Vascular and cardiac hypertrophy were significantly attenuated with losartan or perindopril, but were unchanged with other treatments." | ( Anderson, NH; Devlin, AM; Dominiczak, AF; Graham, D; Hamilton, CA; Morton, JJ; Reid, JL; Schork, NJ, 1999) |
| "Both treatments resulted in cardiac hypertrophy, but only isoproterenol induced significant increases in beta-adrenergic receptor kinase-1 protein levels and activity." | ( Dolber, PC; Iaccarino, G; Koch, WJ; Lefkowitz, RJ, 1999) |
| "Compensated cardiac hypertrophy was induced by abdominal aortic constriction for 5 wk followed by administration of ramipril (50 microg x kg(-1) x day(-1)) or vehicle for 4 wk." | ( Boateng, SY; Boheler, KR; Koban, MU; MacLeod, KT; Naqvi, RU; Yacoub, MH, 2001) |
| "Isoproterenol pretreatment caused cardiac hypertrophy (29%) as shown by a significant increase in the ratio of ventricular dry weight to body weight." | ( Duarte, GP; Lahlou, S; Monteiro-Filho, WO; Silva, CO, 2001) |
| "However, only a partial reduction of cardiac hypertrophy has been successful using current drug therapy." | ( Adachi, S; Hiroe, M; Ito, H; Marum, F; Nozato, T; Ono, Y; Sunamori, M; Tanaka, H; Watanabe, M, 2001) |
| "E(2) treatment reduced cardiac hypertrophy by 31% and 26% compared with placebo 4 and 8 weeks after TAC, whereas it had no effect on the degree of pressure overload, as determined by hemodynamic measurements." | ( Cleutjens, JP; Doevendans, PA; Grohé, C; Janssen, BJ; van Eickels, M; Wellens, HJ, 2001) |
| "Physiological and pathological cardiac hypertrophy have directionally opposite changes in transcription of thyroid hormone (TH)-responsive genes, including alpha- and beta-myosin heavy chain (MyHC) and sarcoplasmic reticulum Ca(2+)-ATPase (SERCA), and TH treatment can reverse molecular and functional abnormalities in pathological hypertrophy, such as pressure overload." | ( Aoyagi, T; Baxter, JD; Bristow, MR; Camacho, SA; Eto, Y; Kinugawa, K; Long, CS; Ribeiro, RC; Simpson, PC; Yonekura, K, 2001) |
| "Indeed, Sim inhibited cardiac hypertrophy and decreased myocardial Rac1 activity and O2*- production in rats treated with AngII infusion or subjected to transaortic constriction." | ( Grimm, M; Kitakaze, M; Liao, JK; Liao, Y; Nakagami, H; Node, K; Takemoto, M; Takemoto, Y, 2001) |
| "Gene expression, accompanied by cardiac hypertrophy, was also suppressed by the FK506 treatment." | ( Hayakawa, T; Hayashi, K; Ito, M; Kamiya, H; Matsui, H; Okumura, K; Saburi, Y; Tomida, T, 2001) |
| "Developmental studies indicated that cardiac hypertrophy was evident as early as 16 days of age in viral vector-treated control transgenic rats, despite these animals exhibiting normal blood pressure." | ( Diz, DM; Ferrario, CM; Katovich, MJ; Numan, MT; Pachori, AS; Raizada, MK, 2002) |
| "The three treatments regressed cardiac hypertrophy and normalized sodium/hydrogen ion exchange exchange activity in SHR, and losartan was the most effective treatment for reversing cardiac hypertrophy, despite producing effects on blood pressure and sodium/hydrogen exchange activity similar to that of other antihypertensive drugs." | ( Alvarez, BV; Cingolani, HE; De Hurtado, MC; Ennis, IL, 2002) |
| "As a model of inhibited cardiac hypertrophy, carnitine-treated JVS (CT) mice were produced." | ( Hayashi, K; Ito, M; Kamiya, H; Matsubara, K; Matsui, H; Okumura, K; Saburi, Y; Takahashi, R, 2003) |
| "We induced cardiac hypertrophy in rats by abdominal aorta stenosis for 12 weeks and thereafter animals were treated for 2 weeks with losartan (12 mg/kg per day), an antagonist of type 1 Ang II receptors (AT1)." | ( Capuano, V; Coulombe, A; Deroubaix, E; Ferron, L; Renaud, JF; Ruchon, Y, 2003) |
| "However, the reduction in cardiac hypertrophy was greater in SHRSP treated with ARB or combination therapy than in those treated with ACEI." | ( Akino, M; Chiba, S; Jia, N; Kitabatake, A; Matsui, Y; Okamoto, H; Shimizu, T; Sugawara, T, 2003) |
| "In conclusion, in a model of cardiac hypertrophy such as that of aortic-banding, increased response to alpha1-adrenergic stimulation is observed, which is blunted by mepivacaine administration." | ( Cokkinos, D; Karageorgiou, C; Kostopanagiotou, G; Mourouzis, C; Mourouzis, I; Pantos, C; Saranteas, T; Tesseromatis, C; Varonos, D, 2003) |
| "Omapatrilat dose-dependently reduced cardiac hypertrophy, caused a greater inhibition of renal ACE than fosinopril, and was the only treatment to inhibit renal NEP." | ( Burrell, LM; Cooper, ME; Jaworski, K; Kubota, E; Mifsud, SA; Wilkinson-Berka, JL, 2004) |
| "dTGR treated with low-dose Val had cardiac hypertrophy (4." | ( Dechend, R; Feldman, DL; Fiebeler, A; Garrelds, IM; Gratze, P; Jan Danser, AH; Luft, FC; Meiners, S; Müller, DN; Pilz, B; Shagdarsuren, E; Webb, RL; Wellner, M, 2005) |
| "The data show that cardiac hypertrophy activated by short-term GH treatment confers cardioprotection compared with pressure overload with regard to molecular and histological characteristics, and responses to ischemia-reperfusion and mechanical stretch." | ( Cittadini, A; De Groot, MC; Di Gianni, A; Di Rella, F; Horn, M; Isgaard, J; Leupold, A; Monti, MG; Napoli, R; Neubauer, S; Palmieri, EA; Saccà, L; Strömer, H, 2006) |
| "These data indicate that the cardiac hypertrophy induced by acute treatment with thyroid hormone precedes the angiogenic process, which probably occurs later." | ( Anjos-Ramos, L; Barreto-Chaves, ML; Carneiro-Ramos, MS; Diniz, GP; Martins-Silva, J, 2006) |
| "In conclusion, these data imply that cardiac hypertrophy associated with chronic administration of rosiglitazone in dogs in previous in vivo studies might be partly attributable to production of the metabolite SB-271258 since this metabolite was shown to elicit trophic effects directly on rat cardiomyocytes." | ( Bell, D; McDermott, BJ, 2006) |
| "SOE-treated ZDF rats showed less cardiac hypertrophy (decrease in weights of the hearts and left ventricles and reduced cardiomyocyte cross-sectional areas)." | ( Harada, M; He, L; Huang, TH; Li, Y; Peng, G; Qi, Y; Qin, Q; Roufogalis, BD; Yamahara, J; Yang, Q, 2008) |
| "l-NAME treatment in wild mice caused cardiac hypertrophy, myocyte apoptosis, macrophage infiltration, coronary arterial remodeling, interstitial fibrosis, and the expression of monocyte chemoattractant protein-1 and transforming growth factor-beta1, whereas these cardiac changes by l-NAME were absent in ASK1-deficient mice." | ( Dong, YF; Ichijo, H; Kataoka, K; Kim-Mitsuyama, S; Matsuba, S; Nakamura, T; Ogawa, H; Tokutomi, Y; Yamamoto, E; Yamashita, T, 2007) |
| "These data indicate that cardiac hypertrophy after PPAR-gamma agonist treatment can occur in the absence of myocardial insulin signaling and is likely secondary to the hemodynamic consequences of plasma volume expansion." | ( Abel, ED; Berger, JP; Litwin, SE; McQueen, AP; Pereira, RO; Rasmussen, IR; Sena, S; Theobald, HA; Wende, AR; Wilde, N, 2007) |
| "In addition, two cardiac hypertrophy marker genes, atrial natriuretic factor and beta-myosin heavy chain, were not up-regulated in E33A-treated cells." | ( Das, B; Gupta, S; Misra, S; Sen, S; Vasanji, A; Xu, Z, 2008) |
| "To assess the role of ET in mediating cardiac hypertrophy and gene expression with high salt, additional groups were treated with an ET(A)/ET(B) receptor antagonist (bosentan) while on high salt." | ( Hoepf, TM; Holycross, BJ; McCune, SA; Radin, MJ, 2008) |
| "Furthermore, after MI LV dilatation, cardiac hypertrophy and lung weights were decreased in mice treated with aliskiren compared with placebo-treated mice after MI." | ( Becher, PM; Escher, F; Jan Danser, AH; Lettau, O; Riad, A; Roks, A; Savvatis, K; Schultheiss, HP; Tschöpe, C; Westermann, D, 2008) |
| "We investigated cardiac hypertrophy elicited by rosiglitazone treatment at the level of protein synthesis/degradation, mTOR, MAPK and AMPK signalling pathways, cardiac function and aspects of carbohydrate/lipid metabolism." | ( Achouba, A; Arsenault, M; Brûlé, S; Couet, J; Deshaies, Y; Festuccia, WT; Guerra-Sá, R; Houde, VP; Lachance, D; Laplante, M; Marette, A; Pedrosa, ML; Silva, ME, 2009) |
| "In isoprenaline-treated rats, cardiac hypertrophy and dysfunction were found." | ( Cheng, YS; Dai, DZ; Dai, Y, 2009) |
| "Treatment with norepinephrine induced cardiac hypertrophy accompanied by G(h) expression and membrane translocation." | ( Cha, MJ; Chang, W; Choi, E; Choi, EY; Chung, N; Hwang, KC; Jang, Y; Kim, HJ; Lim, S; Song, BW, 2010) |
| "Despite displaying cardiac hypertrophy at baseline and higher blood pressure responses to L-NAME/AngII, cav-1 KO mice displayed, as compared with WT, decreased treatment-induced biventricular damage as well as decreased transcript levels of the proinflammatory marker plasminogen activator inhibitor-1." | ( Adler, GK; Coutinho, P; Guo, C; Lapointe, N; Loutraris, P; Pojoga, LH; Ricchiuti, V; Romero, JR; Stone, JR; Williams, GH; Yao, TM, 2010) |
| "KMUP-1 attenuates the cardiac hypertrophy in rats induced by administration of ISO." | ( Chen, IJ; Dai, ZK; Hsu, JH; Liou, SF; Liu, CP; Wu, BN; Wu, JR; Wu, PJ; Yeh, JL, 2010) |
| "The angiotensin II treatment promoted cardiac hypertrophy, concomitant with a significant decrease in cardiac ATRAP expression, but without significant change in cardiac angiotensin II type 1 receptor expression." | ( Bai, Y; Dejima, T; Hirawa, N; Horiuchi, M; Ichihara, N; Ishigami, T; Kobayashi, Y; Maeda, A; Masuda, S; Matsuda, M; Minamisawa, S; Mogi, M; Shigenaga, A; Tamura, K; Tanaka, Y; Toya, Y; Umemura, S; Wakui, H; Yabana, M, 2010) |
| "To arrest the development of cardiac hypertrophy, daily resveratrol treatment (2." | ( Juric, D; Louis, XL; Netticadan, T; Taylor, C; Thandapilly, SJ; Wojciechowski, P; Yu, L, 2010) |
| "Chronic isoproterenol (ISO)-induced cardiac hypertrophy was inhibited in wild-type mice and AT1aR(-/-) mice treated with the ARB Candesartan (CV11974)." | ( Kimura, S; Matsuyoshi, H; Murao, K; Obata, K; Takaki, M; Yu, X; Zhang, GX, 2010) |
| "After abdominal aorta banding to induce cardiac hypertrophy, rats were treated for 8 weeks with apocynin (Apo) or captopril (Cap)." | ( An, W; Lin, Y; Liu, J; Yang, Y; Zang, W; Zhou, J, 2010) |
| "ANG II-induced cardiac hypertrophy was suppressed in mice treated with AdSiR-MR-1, as determined by echocardiography." | ( Dai, W; He, W; Jiang, J; Kong, W; Shang, G; Wang, Y, 2010) |
| "Pioglitazone inhibits cardiac hypertrophy of rats in vitro and in vivo, and may play a role in prevention and treatment of cardiovascular diseases characterized by cardiac hypertrophy in future." | ( Liu, YX; Wu, SM; Ye, P; Zhang, C, 2005) |
| "Vitamin D deficiency is associated with cardiac hypertrophy and heart failure, and vitamin D therapy prevents the progression of cardiac hypertrophy in animal models." | ( Bae, S; Choudhury, S; Kang, PM; Karumanchi, SA; Ke, Q; Kroeger, P; Thadhani, R; Yalamarti, B; Yu, H, 2011) |
| "When left untreated, cardiac hypertrophy commonly progresses to heart failure, one of the leading causes of death in the US." | ( Patterson, C; Portbury, A; Willis, MS, 2011) |
| "The preventive effect of olmesartan on cardiac hypertrophy was blunted by co-administration of a selective Ang-(1-7) antagonist, [D-Ala7]-Ang-(1-7)." | ( Furuno, M; Higaki, J; Horiuchi, M; Inaba, S; Iwai, M; Kanno, H; Mogi, M; Okayama, H; Senba, I, 2011) |
| "ISO-induced cardiac hypertrophy and Erk1/2 activation in Pak-1-KO/ISO were attenuated when the selective Erk1/2 inhibitor FR180204 was administered." | ( Chernoff, J; Ke, Y; Knezevic, I; Lei, M; Monasky, MM; Sheehan, KA; Solaro, RJ; Taglieri, DM; Wang, X; Wolska, BM, 2011) |
| "An in vivo cardiac hypertrophy model established by abdominal aorta banding technique in rats was treated with PMQ in increasing dosages (2." | ( Chen, L; Chen, Y; Han, Y; He, T; Jin, MW; Yang, WQ, 2012) |
| "Isoproterenol treatment induced cardiac hypertrophy and increased collagen content, both of which were normalized by spironolactone treatment." | ( Ballesteros, S; Cachofeiro, V; Davel, AP; de las Heras, N; Lahera, V; Martín-Fernández, B; Miana, M; Rossoni, LV; Valero-Muñoz, M; Vassallo, D, 2012) |
| "On the other hand, cardiac hypertrophy and damage elicited by isoproterenol treatment led to a reduction in Mas expression." | ( Almeida, PW; Braga, VB; Campagnole-Santos, MJ; Coutinho, DC; Dias-Peixoto, MF; Ferreira, AJ; Gomes Filho, A; Greco, L; Guatimosim, S; Lima, RF; Melo, DS; Melo, MB; Santos, RA, 2012) |
| "Finally, cardiac hypertrophy, ventricular remodeling, fibrosis, and increases in myocyte area and brain natriuretic peptide levels observed in angiotensin II-infused mice were reduced in triterpene-treated animals." | ( Bartolomé, MV; Cachofeiro, V; Cordova, C; Delgado, C; Gómez-Hurtado, N; Jurado-López, R; Lahera, V; Martín, R; Martínez-Martínez, E; Miana, M; Nieto, ML; San Román, JA, 2012) |
| "In a pre-clinical model of cardiac hypertrophy and heart failure, we were able to overcome loss of heart function by administering the TRPV1 antagonist BCTC (4-(3-Chloro-2-pyridinyl)-N-[4-(1,1-dimethylethyl)phenyl]-1-piperazinecarboxamide)." | ( Buckley, CL; Horton, JS; Stokes, AJ, 2013) |
| ": Development of cardiac hypertrophy after thyroxin (T4) treatment is well recognized." | ( Elnakish, MT; Hassanain, HH; Janssen, PM; Khan, M; Moldovan, L, 2013) |
| "Furthermore, we observed heart enlargement in the HH 40 embryo following AAPH treatment, where the left ventricle and interventricular septum were found to be thickened in a dose-dependent manner due to myocardiac cell hypertrophy." | ( Abe, K; He, RR; Kurihara, H; Lee, KK; Li, XD; Li, Y; Tsoi, B; Wang, XY; Yang, X; Yi, RN, 2013) |
| "T3 treatment induced cardiac hypertrophy, which was not changed by PD treatment." | ( Barreto-Chaves, ML; da Silva, IB; Gomes, DA; Tavares, FM, 2013) |
| "Models of cardiac hypertrophy were induced by transverse aortic constriction (TAC) or Ang II infusion in the mice in vivo, and by isoproterenol (ISO) or Ang II treatment of H9c2 cells in vitro." | ( Du, Z; Gao, X; Han, H; Hang, P; Huo, R; Jiang, Y; Liu, Y; Lu, Y; Song, H; Sun, L; Wang, C; Wang, S; Wei, L, 2013) |
| "To test the hypothesis that SUN induces cardiac hypertrophy through the modulation of AhR, Wistar albino rats were treated for 15 and 30 days with increasing doses of SUN (25, 50, and 100 mg/kg), whereas at the in vitro level, rat cardiomyocyte H9c2 cells were incubated with SUN (1, 2." | ( Al-Arifi, MN; Ansari, MA; El Gendy, MA; Korashy, HM; Maayah, ZH, 2014) |
| "The beneficial effect of SODB on cardiac hypertrophy seems to be related to the stimulation of endogenous antioxidant defense, suggesting that SODB may be of interest as a dietary supplementation during conventional antihypertensive therapy." | ( Carillon, J; Cristol, JP; Jover, B; Lacan, D; Rouanet, JM; Rugale, C, 2014) |
| "Piceatannol pretreatment suppresses cardiac hypertrophy induced by isoproterenol as assessed by heart weight/body weight ratio, cross-sectional area, and expression of hypertrophic markers." | ( Ahn, Y; Jeong, MH; Kang, W; Kee, HJ; Kim, JH; Lim, KS; Park, S, 2014) |
| "Curcumin treatment reduced cardiac hypertrophy, improved diastolic function and reduced extracellular matrix production, without affecting glycemic control, along with a reduction in TGF-β activity as assessed by Smad7 activation (all p < 0." | ( Advani, A; Advani, SL; Bugyei-Twum, A; Connelly, KA; Kelly, DJ; Thai, K; Zhang, Y, 2014) |
| "Plasma ACE activity and cardiac hypertrophy were comparable with animals treated with enalapril." | ( Bissoli, NS; Boëchat, GA; Brasil, GA; Costa, HB; de Andrade, TU; de Lima, EM; do Nascimento, AM; Endringer, DC; Fronza, M; Lenz, D; Romão, W; Ronchi, SN; Scherer, R, 2015) |
| "Volume-overload cardiac hypertrophy was produced in 7-day-old rabbits via an aorto-caval shunt, after which, the rabbits were treated with or without GW7647 (3 mg/kg per day) for 14 days." | ( Fukushima, A; Huqi, A; Jaswal, JS; Kantor, PF; Keung, W; Lam, VH; Lopaschuk, GD; Onay-Besikci, A; Rebeyka, IM; Tanner, BA; Zhang, L, 2015) |
| "HFD administration elicited obesity, cardiac hypertrophy and systolic dysfunction accompanied with elevated serum levels of blood urea nitrogen (BUN), creatinine, fasting serum glucose (FSG), total cholesterol (TC) and triglyceride." | ( Bao, M; Dai, M; He, W; Lin, D; Tan, T; Wang, W; Wang, X; Wen, Y; Zhang, R; Zhang, Y, 2015) |
| "Genipin treatment attenuated cardiac hypertrophy and the histologic/biochemical changes described above." | ( Dai, CS; Ji, XB; Li, XR; Sun, Q; Wen, P; Yang, JW; Zhou, Y, 2015) |
| "In 4-week-treated rats, physiological cardiac hypertrophy was apparent with an upregulation of α-MHC without any change in myofilament contractile activation." | ( Bupha-Intr, T; Pirompol, P; Teekabut, V; Wattanapermpool, J; Weerachatyanukul, W, 2016) |
| "In a model of cardiac hypertrophy, C57BL/6 mice treated with angiotensin II (A2) had increased BMP signaling in the left ventricle." | ( Bloch, DB; Bloch, KD; Buys, ES; Cheng, J; Ernande, L; Kolodziej, SA; Leyton, PA; Mayeur, C; Rhee, DK; Scherrer-Crosbie, M; Shahid, M; Spagnolli, E; Tainsh, RE; Thoonen, R; Wu, MX; Zapol, WM, 2016) |
| "However, cardiac hypertrophy, evaluated by echocardiography, heart weight, cross-sectional area of cardiomyocytes, and gene expression, was inhibited by only Olm treatment, but not by Hyd." | ( Ichikawa, H; Kimura, Y; Kinjo, T; Narita, I; Nishizaki, K; Okumura, K; Osanai, T; Tanaka, M; Tanno, T; Tomita, H, 2016) |
| "AA protects against cardiac hypertrophy by activating AMPKα, and has the potential to be used for the treatment of heart failure." | ( Dai, J; Liao, HH; Ma, ZG; Tang, QZ; Wei, WY; Xu, SC; Yang, Z; Zhang, WB, 2016) |
| "β-AR overstimulation with associated cardiac hypertrophy and increased vasoconstrictor response to phenylephrine in aorta were modeled in rats by 7-day isoproterenol treatment." | ( Alonso, MJ; Clerici, SP; Davel, AP; Jaffe, IZ; Palacios, R; Rossoni, LV; Vassallo, DV; Victorio, JA, 2016) |
| "The extent of fibrosis during cardiac hypertrophy was determined by histopathology analysis and the results revealed that BDE treatment considerably reduced the fibrosis in the heart." | ( A, P; K G, R; Mathew, AK; Nair, A; Nair, RH; P, SR; S, A; Varghese, MV, 2017) |
| "Atv treatment attenuated cardiac hypertrophy induced by cold exposure; Atv also attenuated the increase of cross-sectional area of cardiomyocytes and cardiac collagen content fraction in mice exposed to cold." | ( Bi, C; Cao, X; Ding, F; Feng, D; Han, Z; Huang, Q; Liang, J; Liu, Y; Ma, W; Pan, Z; Yin, K; Zhang, L, 2017) |
| "AAV8-LDLr gene therapy attenuated cardiac hypertrophy, reduced interstitial and perivascular fibrosis, and decreased lung congestion in TAC mice." | ( Aboumsallem, JP; Amin, R; De Geest, B; Dresselaers, T; Gheysens, O; Himmelreich, U; Jacobs, F; Mishra, M; Muthuramu, I; Postnov, A; Van Veldhoven, PP, 2017) |
| "Sex differences in cardiac hypertrophy were apparent after 3 weeks of treatment." | ( Chen, Y; Fillmore, N; Gao, S; Harrington, J; Liu, P; Murphy, E; Springer, D; Stoehr, A; Wang, X; Yang, Y; Zhang, X; Zhu, J, 2017) |
| "Pathological cardiac hypertrophy is the main determinant of the development of heart failure, for which there is often no effective therapy." | ( Gong, H; Lian, X; Peng, F; Wang, L; Ye, N; Zhang, H, 2018) |
| "In vivo, partial pathological cardiac hypertrophy injuries were relieved after OPD treatment." | ( Chen, X; Gao, Y; Huang, X; Ma, Z; Wang, Y, 2018) |
| "The new role of Tβ4 in cardiac hypertrophy advances our understanding, and the mechanism of action of Tβ4 may provide a solid foundation for the treatment of cardiac disease." | ( Gupta, S; Li, L, 2018) |
| "Additionally, TMAO treatment induced cardiac hypertrophy and cardiac fibrosis in SD rats." | ( Chen, M; Deng, Y; Li, Z; Liu, H; Liu, Q; Ou, C; Wu, Z; Yan, J, 2019) |
| "Rats model of cardiac hypertrophy and fibrosis was induced by isoprenaline (5 mg/kg/day, subcutaneous injection), which were treated with or without curcumin (200 mg/kg/day, intragastric administration)." | ( Li, CL; Liu, JX; Liu, R; Wang, JR; Yang, J; Zhang, HB, 2018) |
| "The high expression of cardiac hypertrophy-linked genes (ANP, β-MHC) was reversed through AA treatment in the hearts of TAC mice." | ( Li, S; Luo, X; Peng, B; Peng, C; Sun, H, 2019) |
| "Untreated pathological cardiac hypertrophy, which can be caused by sustained systemic hypertension, may lead to heart failure." | ( Chen, R; Liu, P; Lu, Y; Qiao, C; Shao, C; Song, J; Wang, L; Wang, Z; Xie, Q; Yan, J; Yang, P, 2019) |
| "Pathological cardiac hypertrophy eventually leads to heart failure without adequate treatment." | ( Bi, HL; Cao, HJ; Han, L; Lai, S; Li, HH; Li, N; Wang, HX; Xie, X; Zhang, YL, 2019) |
| "Rat and H9C2 cell models of cardiac hypertrophy were induced by isoproterenol and angiotensin II, respectively, followed by TUPS treatment." | ( Chen, Y; Liang, J; Pan, R; Wu, F; Wu, G; Wu, Z; Xu, W; Yan, W; Zhang, H; Zhang, K, 2019) |
| "The pathological cardiac hypertrophy will develop into heart failure, which has no effective treatment currently." | ( Feng, YQ; Geng, QS; Hu, ZQ; Huang, L; Huang, YQ; Shan, ZX; Yu, XJ; Zhu, JN, 2019) |
| "Ang II treatment remarkably increased cardiac hypertrophy as indicated by increased ratio of heart weight/body weight and enlarged cardiomyocyte size, extensive fibrosis and inflammation, as well as enhanced expression of hypertrophic markers, whereas hearts from NaBu-treated rats exhibited a significant reduction in these hypertrophic responses." | ( Boini, KM; Chen, Y; Deng, M; Lu, A; Tan, Z; Wang, L; Wu, C; Yang, T; Zhang, L; Zhu, Q, 2019) |
| "A rat model of cardiac hypertrophy was induced by isoproterenol treatment (5 mg·kg-1·day-1) for 4 weeks, with or without ALS treatment at 20 mg·kg-1·day-1." | ( Guo, D; Liu, H; Zhao, Z, 2020) |
| "Sustained cardiac hypertrophy, as previously clarified, serves as a critical initiator of heart failure and therefore is acknowledged as an important factor for heart failure treatment." | ( Cai, K; Chen, H, 2020) |
| "All these cardiac hypertrophy markers were decreased in 'piperine pretreated ISO administered group' compared to group received ISO injection." | ( Aliev, G; Beeraka, NM; Chubarev, VN; Dhivya, V; Gavryushova, LV; Huang, CY; Mikhaleva, LM; Minyaeva, NN; Tarasov, VV; Viswanadha, VP, 2020) |
| "The mRNA levels of cardiac hypertrophy-related genes, atrial natriuretic peptide (ANP) and β-myosin heavy chain (β-MHC), are increased in drug treatment groups." | ( Chen, X; He, H; Shen, Q; Shi, L; Sun, Y; Zhang, L, 2020) |
| "Azilsartan treatment ameliorated cardiac hypertrophy/fibrosis significantly in AAC rats." | ( Cai, SA; Hou, N; Huang, Y; Li, LR; Liu, XW; Luo, CF; Pan, WB; Shi, YY; Yuan, WC; Zhan, HX; Zhao, GJ, 2021) |
| "An in vitro cardiac hypertrophy model and an in vivo heart failure (HF) model induced by isoprenaline (ISO) were established and treated with or without 1,8-CIN." | ( Fu, D; Fu, Y; Gong, G; Wang, Y; Wei, C; Zhang, X; Zhen, D, 2021) |
| "In vitro experiments of cardiac hypertrophy, apoptosis, and aberrant autophagy were performed in cultured cells after Ang II treatment or transfection of miR-128 antagomir." | ( Guo, S; Han, X; Huang, F; Jiao, M; Ma, W; Mi, S; Niu, Q; Zhan, H; Zhang, K; Zhao, Z, 2021) |
| "Rats were injected with ISO to induce cardiac hypertrophy and treated with MCP." | ( Li, AY; Li, Y; Liu, WZ; Liu, XC; Song, QH; Sun, JH; Xu, GR; Yang, HX; Zhang, C; Zhang, Y; Zhou, WW, 2021) |
| "TMAVA treatment aggravated cardiac hypertrophy and dysfunction in high-fat diet-fed mice." | ( Cai, J; Chen, YE; Cheng, S; Cui, X; Dong, E; Gao, J; Garcia-Barrio, MT; Ji, L; Jiang, H; Li, C; Liu, C; Meng, X; Pan, B; Shan, W; Song, M; Sun, H; Wang, DW; Wei, H; Yi, Y; Zhan, R; Zhao, M; Zheng, L, 2022) |
| "We used phenylephrine (PE) to induce cardiac hypertrophy and treated with TCA in vivo and in vitro." | ( Chen, H; Guo, W; Lu, R; Qian, D; Shan, X; Tian, J; Wang, S; Xu, M; Zhang, C; Zhao, P, 2022) |
| "TAC-induced alterations in cardiac hypertrophy markers, histopathological changes, and cardiac function were markedly ameliorated by oral administration of Daph in mice." | ( Kulhari, U; Kumar, A; Kundu, S; Mohapatra, P; Mugale, MN; Murty, US; Ram, C; Sahu, BD; Syed, AM, 2022) |
| "A zebrafish cardiac hypertrophy developed by 500 μM phenylephrine (PE) treatment in ex vivo culture has been demonstrated to activate the essential expression of the embryonal genes." | ( Bertone, R; Bonvissuto, D; Ceci, M; Cervia, D; Gornati, R; Lauri, C; Romano, N; Sette, C; Volpe, V, 2022) |
| "Specific drugs for the treatment of cardiac hypertrophy are still in urgent need." | ( Liu, Y; Ma, F; Wang, Y; Wu, H; Xu, S, 2022) |
| "ISL treatment decreased cardiac hypertrophy and improved cardiac dysfunction induced by pressure overload." | ( Cai, Q; Dong, T; Gao, M; Lv, M; Shi, S; Si, H; Wang, X; Wei, H, 2022) |
| "Pathological cardiac hypertrophy is an independent risk factor for heart failure and is considered a target for the treatment of heart failure." | ( Gao, Y; Guo, X; Hu, L; Li, Y; Liu, Y; Ma, S; Tang, J; Wang, Z; Wei, J; Zhang, Q; Zhang, X; Zhang, Y, 2022) |
| "The model of cardiac hypertrophy was induced by infusion of angiotensin (Ang) II in mice, and was induced by Ang II treatment in neonatal rat cardiomyocyte (NRCM)." | ( Chen, L; Li, Y; Liu, X; Wang, Y; Xing, Y; Zhang, G, 2022) |
| "PE treatment induced the expression of cardiac hypertrophy markers, including natriuretic peptide A (Nppa), natriuretic peptide B (Nppb), and myosin heavy chain 7 (Myh7), in a time-dependent manner in NRVMs." | ( Chen, W; Fang, Y; Guo, N; Guo, Q; Lv, J; Wang, Z; Zeng, S; Zhao, Z, 2023) |
| "After baicalin treatment, cardiac hypertrophy was monitored by detecting the expression of hypertrophic genes and cell surface area." | ( Cai, Y; Craig Wan, C; Du, R; Gao, S; Huang, C; Jiang, S; Shen, A; Xiao, Y; Yan, T; Yang, W; Zhang, X; Zheng, G, 2023) |
| "Pathological cardiac hypertrophy is a major cause of heart failure, and there is no effective approach for its prevention or treatment." | ( Deng, H; Jiang, Z; Liu, H; Liu, X; Ren, Z; Tian, Z; Wu, Z; Zhou, Z, 2023) |
| "Mouse model of pathological cardiac hypertrophy was generated by transverse aortic constriction (TAC) or minipump administration of the β-adrenergic agonist ISO for 4 weeks, and PM (0." | ( Bao, X; Feng, J; Jing, Z; Lu, Y; Wu, M; Zeng, Z, 2023) |
| "Pathological cardiac hypertrophy is a hallmark of various cardiovascular diseases (CVD) including chronic heart failure (HF) and an important target for the treatment of these diseases." | ( Chen, J; Ma, E; Peng, L; Ren, DN; Wo, D; Wu, C; Yan, H; Zhu, W, 2023) |