Key result
Atorvastatin improves cardiac function and inhibits myocardial fibrosis in AMI rats via notch1-TGF-β-smads signaling.
Why the study?
To determine the effects of atorvastatin on cardiac function and hemodynamics and investigate its functional mechanism on cardiac fibrosis in acute myocardial infarction rats.
Does atorvastatin improve cardiac function and reduce myocardial fibrosis in acute myocardial infarction rats?
Does atorvastatin improve cardiac function and reduce myocardial fibrosis in acute myocardial infarction rats?
Atorvastatin mitigates myocardial remodeling and improves cardiac function in a rat model of acute myocardial infarction by interfering with the notch1-TGF-β-smads signaling pathway.
Answers are grounded in this paper and cite their sources.
Hypothesis-generating for statin effects on post-MI fibrosis pathways; should not change clinical practice.
INTRODUCTION: The aim of this study was to determine the effects of atorvastatin on cardiac function and hemodynamics and to investigate its functional mechanism on cardiac fibrosis in acute myocardial infarction (AMI) rats. METHODS: Cardiac functions and hemodynamic changes were evaluated in each group on day 28. Quantitative reverse transcription-polymerase chain reaction, Western blot, and immunohistochemistry were performed to detect the expression of notch1, transforming growth factor-β (TGF-β), Smad2, Smad7, as well as myocardial fibrosis factors (i.e., collagen I, collagen III, and galectin-3) in the myocardial tissues of AMI rats. The changes of myocardial cell structure and myocardial collagen fibers of AMI rats were observed with hematoxylin and eosin staining and Masson staining. RESULTS: Atorvastatin improved the cardiac function and hemodynamic performance. Atorvastatin downregulated the expression of notch1, smad2, collagen I, and collagen III in AMI rats. Atorvastatin treatment decreased the transcription of notch1, TGF-β, and smad2, while it increased smad7 in AMI rats. Atorvastatin induced the downregulation of collagen I, collagen III, and galectin-3. Myocardial immunohistochemical analysis showed atorvastatin inhibited the expression of notch1, TGF-β, and smad2 in myocardial tissues. CONCLUSION: Atorvastatin inhibited myocardial fibrosis by interfering with notch1-TGF-β-smads signal pathways. In addition, it could mitigate myocardial remodeling and improve cardiac functions and hemodynamics.
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Kang et al. (2025) studied Acute myocardial infarction. Atorvastatin was evaluated on Cardiac function, hemodynamics, and myocardial fibrosis. Atorvastatin improved cardiac function and hemodynamics and inhibited myocardial fibrosis in acute myocardial infarction rats by interfering with the notch1-TGF-β-smads signaling pathway.
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