hydroxyproline has been researched along with Left Ventricular Hypertrophy in 31 studies
Hydroxyproline: A hydroxylated form of the imino acid proline. A deficiency in ASCORBIC ACID can result in impaired hydroxyproline formation.
hydroxyproline : A proline derivative that is proline substituted by at least one hydroxy group.
| Excerpt | Relevance | Reference |
|---|---|---|
| "We investigated whether the substrate for nitric oxide synthesis L-arginine is able to modify hypertension and left ventricular hypertrophy development induced by chronic blockade of nitric oxide synthase activity by NG-nitro-L-arginine-methyl ester (L-NAME)." | 7.73 | L-arginine fails to protect against myocardial remodelling in L-NAME-induced hypertension. ( Babal, P; Bernatova, I; Gvozdjakova, A; Krajcirovicova, K; Kucharska, J; Luptak, I; Matuskova, J; Pechanova, O; Simko, F; Simko, J; Sumbalova, Z, 2005) |
| "To investigate the effects of simvastatin (Sim) on left ventricular hypertrophy in rats with pressure-overload cardiac hypertrophy." | 7.70 | Effects of simvastatin on left ventricular hypertrophy and function in rats with aortic stenosis. ( Guan, JX; Liu, XH; Luo, JD; Zhang, GP; Zhang, WW, 1999) |
| "Hexarelin treatment significantly reduced cardiac fibrosis in SHRs by decreasing interstitial and perivascular myocardial collagen deposition and myocardial hydroxyproline content and reducing mRNA and protein expression of collagen I and III in SHR hearts." | 5.38 | Chronic administration of hexarelin attenuates cardiac fibrosis in the spontaneously hypertensive rat. ( Cao, JM; Chen, C; Ding, F; Gao, X; Hao, W; Pang, J; Xu, RK; Xu, X, 2012) |
| "The present study was designed to determine whether atorvastatin reduced hypertension-induced cardiac remodeling and whether these effects involved Protein Kinase D (PKD) and Myocyte Enhancer Factor 2D (MEF2D), factors known to be implicated in cardiac hypertrophy and fibrosis." | 3.76 | Atorvastatin reverses cardiac remodeling possibly through regulation of protein kinase D/myocyte enhancer factor 2D activation in spontaneously hypertensive rats. ( Geng, J; Kang, W; Wang, W; Zhang, Y; Zhao, Z; Zhiming, GE, 2010) |
| " LVH was characterized by increases in the ratios of heart and left ventricular weights to body weight, increased myocyte cross-sectional areas, myocardial and perivascular fibrosis, and elevated cardiac hydroxyproline." | 3.75 | K(ATP) activation prevents progression of cardiac hypertrophy to failure induced by pressure overload via protecting endothelial function. ( Gao, S; Long, CL; Wang, H; Wang, RH, 2009) |
| "Wistar rats were divided into the following 4 groups: 1) C--control (n=13); 2) AoS--aortic stenosis (n=11); 3) LIS--AoS treated with lisinopril, 20 mg/kg/day (n=11); and 4) LOS--AoS treated with losartan, 40 mg/kg/day (n=9)." | 3.73 | [Blockade of renin-angiotensin system attenuates cardiac remodeling in rats undergoing aortic stenosis]. ( Aragon, FF; Cicogna, AC; Cordaro, FR; Gonçalves, G; Okoshi, K; Okoshi, MP; Padovani, CR; Ribeiro, HB; Zornoff, LA, 2005) |
| "We investigated whether the substrate for nitric oxide synthesis L-arginine is able to modify hypertension and left ventricular hypertrophy development induced by chronic blockade of nitric oxide synthase activity by NG-nitro-L-arginine-methyl ester (L-NAME)." | 3.73 | L-arginine fails to protect against myocardial remodelling in L-NAME-induced hypertension. ( Babal, P; Bernatova, I; Gvozdjakova, A; Krajcirovicova, K; Kucharska, J; Luptak, I; Matuskova, J; Pechanova, O; Simko, F; Simko, J; Sumbalova, Z, 2005) |
| "To investigate the effects of simvastatin (Sim) on left ventricular hypertrophy in rats with pressure-overload cardiac hypertrophy." | 3.70 | Effects of simvastatin on left ventricular hypertrophy and function in rats with aortic stenosis. ( Guan, JX; Liu, XH; Luo, JD; Zhang, GP; Zhang, WW, 1999) |
| " Therefore, to evaluate the potential benefit of the angiotensin converting enzyme (ACE) inhibitor quinapril in reversing the interstitial remodeling in spontaneously hypertensive rats (SHR) with established left ventricular hypertrophy (LVH), we treated 16-week-old male SHR with oral quinapril (average dose, 10 mg/kg body weight/day) for 20 weeks." | 3.69 | Quinapril decreases myocardial accumulation of extracellular matrix components in spontaneously hypertensive rats. ( Cenarruzabeitia, E; Díez, J; Galindo, MF; Hernández, M; Panizo, A; Pardo, J, 1995) |
| "Myocyte morphometrics (isolated cell technique) and collagen content (hydroxyproline analysis) were assessed 28 days following experimental myocardial infarction from rats with permanently ligated left coronary vessels (NRP; n = 10) compared with rats who underwent reperfusion 150 minutes after ligation (RP; n = 11) and a sham-operated group (n = 10)." | 3.69 | The effect of delayed reperfusion following infarction in the rat on structural changes in viable myocardium. ( Carlyle, W; Chu, C; Francis, G; Hartman, M; Hauer, K; Judd, D; McDonald, K; Toher, C, 1997) |
| "Hexarelin treatment significantly reduced cardiac fibrosis in SHRs by decreasing interstitial and perivascular myocardial collagen deposition and myocardial hydroxyproline content and reducing mRNA and protein expression of collagen I and III in SHR hearts." | 1.38 | Chronic administration of hexarelin attenuates cardiac fibrosis in the spontaneously hypertensive rat. ( Cao, JM; Chen, C; Ding, F; Gao, X; Hao, W; Pang, J; Xu, RK; Xu, X, 2012) |
| "Pressure-overload left ventricular hypertrophy (LVH) is characterized by an increase in myocyte size and fibrosis." | 1.32 | Reduction of cardiac fibrosis decreases systolic performance without affecting diastolic function in hypertensive rats. ( Carretero, OA; Cingolani, OH; Liu, YH; Rhaleb, NE; Villanueva, M; Yang, XP, 2004) |
| "The transition from compensated left ventricular hypertrophy (LVH) to heart failure is associated with alterations in the myocardial interstitium." | 1.31 | Reduction in myocardial collagen cross-linking parallels left ventricular dilatation in rat models of systolic chamber dysfunction. ( Chung, ES; Lancaster, EJ; Mela, T; Meyer, TE; Norton, GR; Sprott, S; Tsotetsi, OJ; Woodiwiss, AJ, 2001) |
| "Captopril treatment further enhanced pulse pressure by decreasing diastolic blood pressure." | 1.31 | Captopril fails to reverse hypertrophy of the left ventricle induced by aortic insufficiency in rabbits. ( Kyselovic, J; Pelouch, V; Simko, F, 2002) |
| " In the present study, we tested the hypothesis that long-term administration of the hydroxy-3-methylglutaryl coenzyme A (HMG-CoA) reductase inhibitor simvastatin may regress hypertrophy and the possible effect of simvastatin on angiotensin-converting enzyme (ACE) activity in rats with pressure-overload cardiac hypertrophy." | 1.30 | Simvastatin inhibits cardiac hypertrophy and angiotensin-converting enzyme activity in rats with aortic stenosis. ( Chen, X; Guan, JX; Luo, JD; Zhang, GP; Zhang, WW, 1999) |
| "The hydroxyproline content was 5." | 1.30 | [Effects of praeruptorin C on cardiac dysfunction, myocardial compliance and collagen content in renovascular hypertensive rats]. ( Liu, PQ; Rao, MR; Sun, L, 1997) |
| "enalapril-treated group at > or = 15 mm Hg, p < 0." | 1.29 | Comparative effects of type 1 angiotensin II-receptor blockade with angiotensin-converting-enzyme inhibitor on left ventricular distensibility and collagen metabolism in spontaneously hypertensive rats. ( Fujii, A; Katayama, K; Matsuzaki, M; Umemoto, S; Yonezawa, T, 1996) |
| Timeframe | Studies, this research(%) | All Research% |
|---|---|---|
| pre-1990 | 0 (0.00) | 18.7374 |
| 1990's | 17 (54.84) | 18.2507 |
| 2000's | 10 (32.26) | 29.6817 |
| 2010's | 4 (12.90) | 24.3611 |
| 2020's | 0 (0.00) | 2.80 |
| Authors | Studies |
|---|---|
| Rosa, CM | 1 |
| Xavier, NP | 1 |
| Henrique Campos, D | 1 |
| Fernandes, AA | 1 |
| Cezar, MD | 1 |
| Martinez, PF | 1 |
| Cicogna, AC | 4 |
| Gimenes, C | 1 |
| Gimenes, R | 1 |
| Okoshi, MP | 4 |
| Okoshi, K | 3 |
| Chen, Q | 1 |
| Pang, L | 1 |
| Huang, S | 1 |
| Lei, W | 1 |
| Huang, D | 1 |
| Gao, S | 1 |
| Long, CL | 1 |
| Wang, RH | 1 |
| Wang, H | 1 |
| Geng, J | 1 |
| Zhao, Z | 1 |
| Kang, W | 1 |
| Wang, W | 1 |
| Zhang, Y | 1 |
| Zhiming, GE | 1 |
| Xu, X | 1 |
| Ding, F | 1 |
| Pang, J | 1 |
| Gao, X | 1 |
| Xu, RK | 1 |
| Hao, W | 1 |
| Cao, JM | 1 |
| Chen, C | 1 |
| McGowan, BS | 1 |
| Scott, CB | 1 |
| Mu, A | 1 |
| McCormick, RJ | 1 |
| Thomas, DP | 1 |
| Margulies, KB | 1 |
| Ribeiro, HB | 2 |
| Bregagnollo, EA | 1 |
| Rodrigues, MA | 1 |
| Padovani, CR | 2 |
| Aragon, FF | 2 |
| Jamas, E | 1 |
| Cingolani, OH | 1 |
| Yang, XP | 1 |
| Liu, YH | 1 |
| Villanueva, M | 1 |
| Rhaleb, NE | 1 |
| Carretero, OA | 1 |
| Itter, G | 1 |
| Jung, W | 1 |
| Juretschke, P | 1 |
| Schoelkens, BA | 1 |
| Linz, W | 1 |
| Gonçalves, G | 1 |
| Zornoff, LA | 1 |
| Cordaro, FR | 1 |
| Simko, F | 3 |
| Luptak, I | 1 |
| Matuskova, J | 1 |
| Krajcirovicova, K | 1 |
| Sumbalova, Z | 1 |
| Kucharska, J | 2 |
| Gvozdjakova, A | 2 |
| Simko, J | 1 |
| Babal, P | 1 |
| Pechanova, O | 1 |
| Bernatova, I | 1 |
| Varagic, J | 1 |
| Frohlich, ED | 2 |
| Susic, D | 2 |
| Ahn, J | 1 |
| Matavelli, L | 1 |
| López, B | 1 |
| Díez, J | 3 |
| Laviades, C | 1 |
| Monreal, I | 1 |
| Gil, MJ | 1 |
| Panizo, A | 2 |
| Pardo, J | 2 |
| Hernández, M | 1 |
| Galindo, MF | 1 |
| Cenarruzabeitia, E | 1 |
| Young, M | 1 |
| Fullerton, M | 1 |
| Dilley, R | 1 |
| Funder, J | 1 |
| Brilla, CG | 1 |
| Matsubara, LS | 2 |
| Weber, KT | 1 |
| Yonezawa, T | 1 |
| Umemoto, S | 1 |
| Fujii, A | 1 |
| Katayama, K | 1 |
| Matsuzaki, M | 1 |
| Qi, M | 1 |
| Shannon, TR | 1 |
| Euler, DE | 1 |
| Bers, DM | 1 |
| Samarel, AM | 1 |
| Jugdutt, BI | 1 |
| Lucas, A | 1 |
| Khan, MI | 1 |
| McDonald, K | 1 |
| Chu, C | 1 |
| Francis, G | 1 |
| Judd, D | 1 |
| Carlyle, W | 1 |
| Toher, C | 1 |
| Hauer, K | 1 |
| Hartman, M | 1 |
| Matsubara, BB | 1 |
| Franco, M | 1 |
| Nunez, E | 1 |
| Hosoya, K | 1 |
| Woodiwiss, AJ | 2 |
| Oosthuyse, T | 1 |
| Norton, GR | 2 |
| Turcani, M | 1 |
| Jacob, R | 1 |
| Clair, MJ | 1 |
| Krombach, RS | 1 |
| Coker, ML | 1 |
| Heslin, TL | 1 |
| Kribbs, SB | 1 |
| de Gasparo, M | 1 |
| Spinale, FG | 1 |
| Braunova, Z | 1 |
| Bada, V | 1 |
| Kyselovic, J | 2 |
| Luo, JD | 2 |
| Zhang, WW | 2 |
| Zhang, GP | 2 |
| Liu, XH | 1 |
| Guan, JX | 2 |
| Chen, X | 1 |
| Tsotetsi, OJ | 1 |
| Sprott, S | 1 |
| Lancaster, EJ | 1 |
| Mela, T | 1 |
| Chung, ES | 1 |
| Meyer, TE | 1 |
| Sun, L | 1 |
| Rao, MR | 1 |
| Liu, PQ | 1 |
| Pelouch, V | 1 |
1 review available for hydroxyproline and Left Ventricular Hypertrophy
| Article | Year |
|---|---|
Toward the biochemical assessment of myocardial fibrosis in hypertensive patients.
Topics: Animals; Arrhythmias, Cardiac; Biochemical Phenomena; Biochemistry; Biomarkers; Endomyocardial Fibro | 1995 |
30 other studies available for hydroxyproline and Left Ventricular Hypertrophy
| Article | Year |
|---|---|
Diabetes mellitus activates fetal gene program and intensifies cardiac remodeling and oxidative stress in aged spontaneously hypertensive rats.
Topics: Animals; Atrial Natriuretic Factor; Cardiac Myosins; Diabetes Mellitus, Experimental; Diabetic Cardi | 2013 |
Effects of emodin and irbesartan on ventricular fibrosis in Goldblatt hypertensive rats.
Topics: Angiotensin II; Angiotensin II Type 1 Receptor Blockers; Animals; Biphenyl Compounds; Blotting, West | 2014 |
K(ATP) activation prevents progression of cardiac hypertrophy to failure induced by pressure overload via protecting endothelial function.
Topics: Animals; Aorta, Abdominal; Atrial Natriuretic Factor; Blood Pressure; Cardiovascular Agents; Disease | 2009 |
Atorvastatin reverses cardiac remodeling possibly through regulation of protein kinase D/myocyte enhancer factor 2D activation in spontaneously hypertensive rats.
Topics: Animals; Atorvastatin; Blood Pressure; Disease Models, Animal; Enzyme Activation; Fibrosis; Heptanoi | 2010 |
Chronic administration of hexarelin attenuates cardiac fibrosis in the spontaneously hypertensive rat.
Topics: Animals; Blood Pressure; Cardiovascular Agents; Collagen Type I; Collagen Type III; Disease Models, | 2012 |
Unloading-induced remodeling in the normal and hypertrophic left ventricle.
Topics: Algorithms; Amino Acids; Animals; Blotting, Western; Cell Separation; Echocardiography; Gelatin; Hea | 2003 |
Follow-up study of morphology and cardiac function in rats undergoing induction of supravalvular aortic stenosis.
Topics: Analysis of Variance; Animals; Aortic Stenosis, Supravalvular; Disease Models, Animal; Echocardiogra | 2003 |
Reduction of cardiac fibrosis decreases systolic performance without affecting diastolic function in hypertensive rats.
Topics: Animals; Capillaries; Cell Size; Collagen; Diastole; Fibrosis; Heart Ventricles; Hydroxyproline; Hyp | 2004 |
A model of chronic heart failure in spontaneous hypertensive rats (SHR).
Topics: Animals; Aorta; Blood Pressure; Disease Models, Animal; Heart Failure; Heart Rate; Hydroxyproline; H | 2004 |
[Blockade of renin-angiotensin system attenuates cardiac remodeling in rats undergoing aortic stenosis].
Topics: Angiotensin II Type 1 Receptor Blockers; Angiotensin-Converting Enzyme Inhibitors; Animals; Aortic V | 2005 |
L-arginine fails to protect against myocardial remodelling in L-NAME-induced hypertension.
Topics: Animals; Antihypertensive Agents; Arginine; Brain; Hydroxyproline; Hypertension; Hypertrophy, Left V | 2005 |
AT1 receptor antagonism attenuates target organ effects of salt excess in SHRs without affecting pressure.
Topics: Angiotensin II Type 1 Receptor Blockers; Animals; Aorta, Thoracic; Blood Pressure; Body Weight; Coro | 2008 |
Quinapril decreases myocardial accumulation of extracellular matrix components in spontaneously hypertensive rats.
Topics: Angiotensin-Converting Enzyme Inhibitors; Animals; Antihypertensive Agents; Blood Pressure; Collagen | 1995 |
Mineralocorticoids, hypertension, and cardiac fibrosis.
Topics: Aldosterone; Animals; Blood Pressure; Collagen; Desoxycorticosterone; Endomyocardial Fibrosis; Hydro | 1994 |
Anti-aldosterone treatment and the prevention of myocardial fibrosis in primary and secondary hyperaldosteronism.
Topics: Angiotensin II; Animals; Blood Pressure; Fibrosis; Heart; Hydroxyproline; Hyperaldosteronism; Hypert | 1993 |
Comparative effects of type 1 angiotensin II-receptor blockade with angiotensin-converting-enzyme inhibitor on left ventricular distensibility and collagen metabolism in spontaneously hypertensive rats.
Topics: Angiotensin Receptor Antagonists; Angiotensin-Converting Enzyme Inhibitors; Animals; Collagen; Enala | 1996 |
Downregulation of sarcoplasmic reticulum Ca(2+)-ATPase during progression of left ventricular hypertrophy.
Topics: Animals; Biological Transport, Active; Calcium; Calcium-Transporting ATPases; Diastole; Down-Regulat | 1997 |
Effect of angiotensin-converting enzyme inhibition on infarct collagen deposition and remodelling during healing after transmural canine myocardial infarction.
Topics: Angiotensin-Converting Enzyme Inhibitors; Animals; Captopril; Collagen; Dogs; Enalapril; Heart Ventr | 1997 |
The effect of delayed reperfusion following infarction in the rat on structural changes in viable myocardium.
Topics: Animals; Cell Nucleus; Cell Size; Hydroxyproline; Hypertrophy, Left Ventricular; Microscopy, Confoca | 1997 |
Myocardial fibrosis rather than hypertrophy induces diastolic dysfunction in renovascular hypertensive rats.
Topics: Angiotensin-Converting Enzyme Inhibitors; Animals; Fibrosis; Heart; Hydroxyproline; Hypertension, Re | 1997 |
Coronary hemodynamics in aging spontaneously hypertensive and normotensive Wistar-Kyoto rats.
Topics: Aging; Animals; Aorta; Body Weight; Collagen; Coronary Circulation; Fibrosis; Hemodynamics; Hydroxyp | 1998 |
Reduced cardiac stiffness following exercise is associated with preserved myocardial collagen characteristics in the rat.
Topics: Animals; Collagen; Diastole; Elasticity; Heart; Hydroxyproline; Hypertrophy, Left Ventricular; Male; | 1998 |
Minoxidil accelerates heart failure development in rats with ascending aortic constriction.
Topics: Animals; Aorta; Collagen; Constriction, Pathologic; Heart; Heart Failure; Hydroxyproline; Hypertroph | 1998 |
Angiotensin AT1 receptor inhibition in pacing induced heart failure: effects on left ventricular myocardial collagen content and composition.
Topics: Animals; Cardiac Pacing, Artificial; Collagen; Echocardiography; Heart Failure; Humans; Hydroxyproli | 1998 |
Passive smoking induced hypertrophy of the left ventricle: effect of captopril.
Topics: Angiotensin-Converting Enzyme Inhibitors; Animals; Body Weight; Captopril; Hydroxyproline; Hypertrop | 1999 |
Effects of simvastatin on left ventricular hypertrophy and function in rats with aortic stenosis.
Topics: Animals; Aortic Valve Stenosis; Hydroxymethylglutaryl-CoA Reductase Inhibitors; Hydroxyproline; Hype | 1999 |
Simvastatin inhibits cardiac hypertrophy and angiotensin-converting enzyme activity in rats with aortic stenosis.
Topics: Angiotensin II; Angiotensin-Converting Enzyme Inhibitors; Animals; Aorta, Abdominal; Blood Pressure; | 1999 |
Reduction in myocardial collagen cross-linking parallels left ventricular dilatation in rat models of systolic chamber dysfunction.
Topics: Angiotensin-Converting Enzyme Inhibitors; Animals; Aorta, Abdominal; Body Weight; Captopril; Collage | 2001 |
[Effects of praeruptorin C on cardiac dysfunction, myocardial compliance and collagen content in renovascular hypertensive rats].
Topics: Animals; Calcium Channel Blockers; Collagen; Coumarins; Heart Function Tests; Hydroxyproline; Hypert | 1997 |
Captopril fails to reverse hypertrophy of the left ventricle induced by aortic insufficiency in rabbits.
Topics: Angiotensin-Converting Enzyme Inhibitors; Animals; Antihypertensive Agents; Aortic Valve Insufficien | 2002 |