hydroxyproline has been researched along with Ventricular Dysfunction, Left in 10 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.
Ventricular Dysfunction, Left: A condition in which the LEFT VENTRICLE of the heart was functionally impaired. This condition usually leads to HEART FAILURE; MYOCARDIAL INFARCTION; and other cardiovascular complications. Diagnosis is made by measuring the diminished ejection fraction and a depressed level of motility of the left ventricular wall.
| Excerpt | Relevance | Reference |
|---|---|---|
| " Thus, we evaluated the effects of atorvastatin on cardiac function, remodeling, fibrosis, and apoptosis after myocardial infarction (MI)." | 7.77 | Atorvastatin therapy during the peri-infarct period attenuates left ventricular dysfunction and remodeling after myocardial infarction. ( Bi, Q; Bolli, R; Dawn, B; Hunt, G; Peng, Y; Sanganalmath, SK; Sato, H; Shirk, G; Tang, XL; Vincent, RJ, 2011) |
| "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) |
| " Thus, we evaluated the effects of atorvastatin on cardiac function, remodeling, fibrosis, and apoptosis after myocardial infarction (MI)." | 3.77 | Atorvastatin therapy during the peri-infarct period attenuates left ventricular dysfunction and remodeling after myocardial infarction. ( Bi, Q; Bolli, R; Dawn, B; Hunt, G; Peng, Y; Sanganalmath, SK; Sato, H; Shirk, G; Tang, XL; Vincent, RJ, 2011) |
| "To determine whether therapy with the angiotensin II type 1 receptor blocker (ARB) candesartan and the comparator angiotensin-converting-enzyme inhibitor (ACEI) enalapril during healing after reperfused ST-elevation myocardial infarction (RSTEMI) limit adverse remodeling of infarct zone (IZ) collagens and left ventricular (LV) diastolic dysfunction, we randomized 24 dogs surviving anterior RSTEMI (90-min coronary occlusion) to placebo, candesartan, and enalapril therapy between day 2 and 42." | 3.74 | Angiotensin receptor blockade and angiotensin-converting-enzyme inhibition limit adverse remodeling of infarct zone collagens and global diastolic dysfunction during healing after reperfused ST-elevation myocardial infarction. ( Idikio, H; Jugdutt, BI; Uwiera, RR, 2007) |
| "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) |
| "Cardioprotective effects of HGF for idiopathic dilated cardiomyopathy were examined in hamsters with electroporation of plasmid DNA into skeletal muscle." | 1.32 | Treatment of dilated cardiomyopathy with electroporation of hepatocyte growth factor gene into skeletal muscle. ( Kangawa, K; Kitakaze, M; Kitamura, S; Komamura, K; Matsumoto, K; Miyatake, K; Miyazaki, J; Nakamura, T; Nakatani, T; Shimizu, Y; Tatsumi, R; Tomoike, H; Yamato, E, 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) |
| Timeframe | Studies, this research(%) | All Research% |
|---|---|---|
| pre-1990 | 0 (0.00) | 18.7374 |
| 1990's | 1 (10.00) | 18.2507 |
| 2000's | 6 (60.00) | 29.6817 |
| 2010's | 3 (30.00) | 24.3611 |
| 2020's | 0 (0.00) | 2.80 |
| Authors | Studies |
|---|---|
| Minicucci, MF | 1 |
| Santos, PP | 1 |
| Rafacho, BP | 1 |
| Gonçalves, AF | 1 |
| Ardisson, LP | 1 |
| Batista, DF | 1 |
| Azevedo, PS | 1 |
| Polegato, BF | 1 |
| Okoshi, K | 1 |
| Pereira, EJ | 1 |
| Paiva, SA | 1 |
| Zornoff, LA | 1 |
| French, CJ | 1 |
| Zaman, AK | 1 |
| Sobel, BE | 1 |
| Tang, XL | 1 |
| Sanganalmath, SK | 1 |
| Sato, H | 1 |
| Bi, Q | 1 |
| Hunt, G | 1 |
| Vincent, RJ | 1 |
| Peng, Y | 1 |
| Shirk, G | 1 |
| Dawn, B | 1 |
| Bolli, R | 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 |
| Komamura, K | 1 |
| Tatsumi, R | 1 |
| Miyazaki, J | 1 |
| Matsumoto, K | 1 |
| Yamato, E | 1 |
| Nakamura, T | 1 |
| Shimizu, Y | 1 |
| Nakatani, T | 1 |
| Kitamura, S | 1 |
| Tomoike, H | 1 |
| Kitakaze, M | 1 |
| Kangawa, K | 1 |
| Miyatake, K | 1 |
| Du, XJ | 1 |
| Gao, XM | 1 |
| Kiriazis, H | 1 |
| Moore, XL | 1 |
| Ming, Z | 1 |
| Su, Y | 1 |
| Finch, AM | 1 |
| Hannan, RA | 1 |
| Dart, AM | 1 |
| Graham, RM | 1 |
| Jugdutt, BI | 1 |
| Idikio, H | 1 |
| Uwiera, RR | 1 |
| Díez, J | 1 |
| Laviades, C | 1 |
| Monreal, I | 1 |
| Gil, MJ | 1 |
| Panizo, A | 1 |
| Pardo, J | 1 |
| Woodiwiss, AJ | 1 |
| Tsotetsi, OJ | 1 |
| Sprott, S | 1 |
| Lancaster, EJ | 1 |
| Mela, T | 1 |
| Chung, ES | 1 |
| Meyer, TE | 1 |
| Norton, GR | 1 |
| Yamamoto, K | 1 |
| Masuyama, T | 1 |
| Sakata, Y | 1 |
| Nishikawa, N | 1 |
| Mano, T | 1 |
| Yoshida, J | 1 |
| Miwa, T | 1 |
| Sugawara, M | 1 |
| Yamaguchi, Y | 1 |
| Ookawara, T | 1 |
| Suzuki, K | 1 |
| Hori, M | 1 |
1 review available for hydroxyproline and Ventricular Dysfunction, Left
| Article | Year |
|---|---|
Toward the biochemical assessment of myocardial fibrosis in hypertensive patients.
Topics: Animals; Arrhythmias, Cardiac; Biochemical Phenomena; Biochemistry; Biomarkers; Endomyocardial Fibro | 1995 |
9 other studies available for hydroxyproline and Ventricular Dysfunction, Left
| Article | Year |
|---|---|
Periostin as a modulator of chronic cardiac remodeling after myocardial infarction.
Topics: Animals; Blotting, Western; Cell Adhesion Molecules; Collagen Type I; Collagen Type III; Diastole; D | 2013 |
Cardiac fibrosis and diastolic dysfunction after myocardial infarction in apolipoprotein E knockout mice.
Topics: Animals; Apolipoproteins E; Body Weight; Diastole; Disease Models, Animal; Echocardiography, Doppler | 2009 |
Atorvastatin therapy during the peri-infarct period attenuates left ventricular dysfunction and remodeling after myocardial infarction.
Topics: Animals; Apoptosis; Atorvastatin; Female; Heptanoic Acids; Hydroxymethylglutaryl-CoA Reductase Inhib | 2011 |
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 |
Treatment of dilated cardiomyopathy with electroporation of hepatocyte growth factor gene into skeletal muscle.
Topics: Animals; Cardiomyopathy, Dilated; Cricetinae; Electroporation; Fibrosis; Genetic Therapy; Genetic Ve | 2004 |
Transgenic alpha1A-adrenergic activation limits post-infarct ventricular remodeling and dysfunction and improves survival.
Topics: Actins; Aging; Animals; Atrial Natriuretic Factor; Collagen; Echocardiography; Female; Fibronectins; | 2006 |
Angiotensin receptor blockade and angiotensin-converting-enzyme inhibition limit adverse remodeling of infarct zone collagens and global diastolic dysfunction during healing after reperfused ST-elevation myocardial infarction.
Topics: Angiotensin II Type 1 Receptor Blockers; Angiotensin Receptor Antagonists; Angiotensin-Converting En | 2007 |
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 |
Myocardial stiffness is determined by ventricular fibrosis, but not by compensatory or excessive hypertrophy in hypertensive heart.
Topics: Analysis of Variance; Angiotensin Receptor Antagonists; Animals; Benzimidazoles; Biphenyl Compounds; | 2002 |