Key result
Atorvastatin reduces SBP and prevents myocardial fibrosis in hypertensive rats by suppressing IL-6/STAT3/ET-1 signaling.
Why the study?
Myocardial fibrosis is an important adverse effect of hypertension, and the roles of the IL-6/STAT3 pathway and ET-1 in myocardial fibrosis require further investigation.
Answers are grounded in this paper and cite their sources.
BACKGROUND Hypertension is a leading global disease, and myocardial fibrosis is an important adverse effect of hypertension, seriously threatening human health. The IL-6/STAT3 pathway and endothelin-1 (ET-1) were previously suggested to play a part in myocardial fibrosis. MATERIAL AND METHODS To investigate the role of Atorvastatin (Ato) in spontaneous hypertension, systolic blood pressure (SBP) and left ventricular mass index (LVMI) were measured, and Masson trichrome staining was performed. Furthermore, the relative protein levels of the IL-6/STAT3/ET-1 pathway were tested. RESULTS Ato prevented myocardial fibrosis in spontaneous hypertension rats, especially at the dosage of 50 mg/kg/d. The IL-6/STAT3 pathway was observed to be suppressed by Ato, and ET-1 level in myocardial tissues was also downregulated by Ato. The phosphorylation status of STAT3 was tested after Ato treatment, showing that Ato mainly stimulated the tyr-705 phosphorylation of STAT3. CONCLUSIONS Results of this study may help promote myocardial fibrosis therapy and provide insights into the IL-6/STAT3/ET-1-mediated mechanism in Ato-induced myocardial fibrosis inhibition.
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Fang et al. (2019) studied Spontaneous hypertension and myocardial fibrosis (n=40). Atorvastatin vs. Distilled water was evaluated on Myocardial fibrosis, systolic blood pressure, and left ventricular mass index (p=<0.001). Atorvastatin significantly reduced systolic blood pressure and prevented myocardial fibrosis in spontaneously hypertensive rats, primarily by suppressing the IL-6/STAT3/ET-1 signaling pathway.
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