The DOI matches its Crossref record; 26 of the 26 references it cites were found in a registry or an index.
Simvastatin Induces Regression of Cardiac Hypertrophy and Fibrosis and Improves Cardiac Function in a Transgenic Rabbit Model of Human Hypertrophic Cardiomyopathy
Open accessAbstract
Background Hypertrophic cardiomyopathy is a genetic disease characterized by cardiac hypertrophy, myocyte disarray, interstitial fibrosis, and left ventricular (LV) dysfunction. We have proposed that hypertrophy and fibrosis, the major determinants of mortality and morbidity, are potentially reversible. We tested this hypothesis in β-myosin heavy chain–Q 403 transgenic rabbits. Methods and Results We randomized 24 β-myosin heavy chain–Q 403 rabbits to treatment with either a placebo or simvastatin (5 mg · kg −1 · d −1 ) for 12 weeks and included 12 nontransgenic controls. We performed 2D and Doppler echocardiography and tissue Doppler imaging before and after treatment. Demographic data were similar among the groups. Baseline mean LV mass and interventricular septal thickness in nontransgenic, placebo, and simvastatin groups were 3.9±0.7, 6.2±2.0, and 7.5±2.1 g ( P <0.001) and 2.2±0.2, 3.1±0.5, and 3.3±0.5 mm ( P =0.002), respectively. Simvastatin reduced LV mass by 37%, interventricular septal thickness by 21%, and posterior wall thickness by 13%. Doppler indices of LV filling pressure were improved. Collagen volume fraction was reduced by 44% ( P <0.001). Disarray was unchanged. Levels of activated extracellular signal-regulated kinase (ERK) 1/2 were increased in the placebo group and were less than normal in the simvastatin group. Levels of activated and total p38, Jun N-terminal kinase, p70S6 kinase, Ras, Rac, and RhoA and the membrane association of Ras, RhoA, and Rac1 were unchanged. Conclusions Simvastatin induced the regression of hypertrophy and fibrosis, improved cardiac function, and reduced ERK1/2 activity in the β-myosin heavy chain–Q 403 rabbits. These findings highlight the need for clinical trials to determine the effects of simvastatin on cardiac hypertrophy, fibrosis, and dysfunction in humans with hypertrophic cardiomyopathy and heart failure.
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Cites
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Increased left ventricular mass and hypertrophy are associated with increased risk for sudden death
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The Molecular Genetic Basis for Hypertrophic Cardiomyopathy
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Cited by
Gersh, B. J., Maron, B. J., Bonow, R. O., Dearani, J. A., Fifer, M. A., Link, M. S., Naidu, S. S., Nishimura, R. A., Ommen, S. R., Rakowski, H., et al. (2011) · Circulation · doi:10.1161/cir.0b013e318223e2bd · Cited by 2,104
Molecular and cellular mechanisms of liver fibrosis and its regression
Kisseleva, T., & Brenner, D. (2021) · Nature Reviews Gastroenterology & Hepatology · doi:10.1038/s41575-020-00372-7 · Cited by 2,024
Hypertrophic Cardiomyopathy: Genetics, Pathogenesis, Clinical Manifestations, Diagnosis, and Therapy
Marian, A. J., & Braunwald, E. (2017) · Circulation Research · doi:10.1161/circresaha.117.311059 · Cited by 1,403
Self-citation2011 ACCF/AHA Guideline for the Diagnosis and Treatment of Hypertrophic Cardiomyopathy
Gersh, B. J., Maron, B. J., Bonow, R. O., Dearani, J. A., Fifer, M. A., Link, M. S., Naidu, S. S., Nishimura, R. A., Ommen, S. R., Rakowski, H., et al. (2011) · Journal of the American College of Cardiology · doi:10.1016/j.jacc.2011.06.011 · Cited by 1,276
Garcia-Gras, E. (2006) · Journal of Clinical Investigation · doi:10.1172/jci27751 · Cited by 623
Metadata
- Authors
- Patel, R., Nagueh, S. F., Tsybouleva, N., Abdellatif, M., Lutucuta, S., Kopelen, H. A., Quinones, M. A., Zoghbi, W. A., Entman, M. L., Roberts, R., & Marian, A. J.
- Venue
- Circulation
- Published
- 2001-07-17
- Volume
- 104
- Issue
- 3
- Pages
- 317-324
- ISSN
- 0009-7322 (ISSN-L)
- 1524-4539
- OpenAlex
- W2120194464
- Cited by
- 357
- References
- 26
- FWCI
- 17.23
- Type
- journal article
- Language
- en
- Open access
- bronze
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- Patel, R., Nagueh, S. F., Tsybouleva, N., Abdellatif, M., Lutucuta, S., Kopelen, H. A., Quinones, M. A., Zoghbi, W. A., Entman, M. L., Roberts, R., & Marian, A. J. (2001). Simvastatin Induces Regression of Cardiac Hypertrophy and Fibrosis and Improves Cardiac Function in a Transgenic Rabbit Model of Human Hypertrophic Cardiomyopathy. Circulation. https://doi.org/10.1161/01.cir.104.3.317
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Contains information from the Semantic Scholar Academic Graph Datasets, made available under the ODC Attribution License (ODC-BY 1.0).
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