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Updated: Jul 14, 2026
Studying Left Ventricular Reverse Remodeling by Aortic Debanding in Rodents
Published on: July 14, 2021
Beneficial effect of atorvastatin on left ventricular remodeling in spontaneously hypertensive rats
Lan Kang1, Chang-Jiang Ge, Shen-Jiang Hu
1Institute of Cardiology, First Affiliated Hospital, College of Medicine, Zhejiang University, Hangzhou, PR China.
Insights
Atorvastatin treatment improved cardiac structure and reduced fibrosis in spontaneously hypertensive rats. This beneficial effect on cardiac remodeling is linked to increased cell apoptosis and p27 protein expression.
Area of Science:
- Cardiovascular Research
- Pharmacology
- Molecular Biology
Background:
- Spontaneously hypertensive rats (SHR) exhibit adverse left ventricular (LV) remodeling, including hypertrophy and fibrosis.
- Understanding the mechanisms behind LV remodeling is crucial for developing effective therapeutic strategies.
- Atorvastatin, a statin drug, is known for its lipid-lowering effects, but its impact on cardiac remodeling requires further investigation.
Purpose of the Study:
- To investigate the beneficial effects of atorvastatin on left ventricular (LV) remodeling in spontaneously hypertensive rats (SHR).
- To explore the underlying molecular mechanisms, including cell apoptosis and p27 protein expression, involved in atorvastatin's action on cardiac remodeling.
Main Methods:
- 12 SHRs were randomized into two groups: one receiving distilled water (SHR group) and the other atorvastatin (ATV group) for 10 weeks.
- Age-matched Wistar-Kyoto rats (WKY) served as normal controls.
- Measurements included cardiosomatic ratio, LV weight to body weight ratio, cardiomyocyte transverse diameter, myocardial hydroxyproline and collagen content, cell apoptosis rate, p27 protein expression, serum lipid concentration, and systolic blood pressure.
Main Results:
- Atorvastatin treatment significantly reduced cardiosomatic ratio, LV weight to body weight ratio, and cardiomyocyte transverse diameter in SHR.
- Myocardial hydroxyproline and collagen content were decreased in atorvastatin-treated SHR, indicating reduced fibrosis.
- Atorvastatin increased the positive rate of cell apoptosis and p27 protein expression in the myocardium.
- Serum lipid concentration and systolic blood pressure were significantly reduced in the atorvastatin-treated SHR group.
Conclusions:
- Atorvastatin demonstrates a beneficial effect on adverse left ventricular remodeling in spontaneously hypertensive rats.
- The induction of cell apoptosis and upregulation of p27 protein are identified as potential underlying mechanisms for atorvastatin's cardioprotective effects.
- These findings suggest atorvastatin may be a valuable therapeutic agent for managing cardiac remodeling in hypertensive conditions.
Abstract:
This study was designed to investigate whether atorvastatin has a beneficial effect on left ventricular (LV) remodeling in spontaneously hypertensive rats (SHR), and then explore the underlying mechanisms involved. 12 SHRs were randomized to receive either distilled water (SHR group, n = 6) or atorvastatin (ATV group, n = 6) for 10 weeks. Age-matched Wistar-Kyoto rats (WKY) gavaged by distilled water were used as normal controls (WKY group, n = 6). By using these rats, we observed the effects of atorvastatin on LV hypertrophy and fibrosis, and investigated atorvastatin-induced cell apoptosis and p27 protein expression. In addition, the serum lipid concentration and blood pressure level were also measured in this study. 10 weeks later, a significant decrease in the cardiosomatic ratio, LV weight to body weight ratio and cardiomyocyte transverse diameter, as well as myocardial hydroxyproline and collagen content was observed in the atorvastatin-treated SHR. In addition, atorvastatin increased the positive rate of cell apoptosis and p27 protein expression. A decreased serum lipid concentration and a reduced systolic blood pressure level were also found in the atorvastatin-treated SHR. These findings demonstrated a beneficial effect of atorvastatin on adverse LV remodeling in SHR, and the induction of cell apoptosis and upregulation of p27 protein may serve as the underlying mechanisms of this action.
