Myocardial infarction (MI) is the most prevalent disease with high mortality, leading to devastating heart injury. Here, we aimed to explore the effect of MAS1 on the MI-induced myocardial injury. Significantly, we identified that the expression of MAS1 was decreased in the MI rat model and hypoxia and reoxygenation (H/R)-treated H9C2 cells. Hematoxylin & Eosin (H&E) staining revealed that the overexpression of MAS1 notably attenuated MI-related myocardium injury in the MI rat model. Echocardiography analysis revealed that MI inhibited left ventricular ejection fraction (LVEF) and left ventricular fraction shortening (LVFS), whereas the MAS1 overexpression could increase LVEF and LVFS in the MI rats. Meanwhile, the expression of collagen I, collagen III, α-SMA, ANP, and BNP was decreased by MAS1 overexpression in the MI rats. MAS1 attenuated cardiomyocyte apoptosis in vivo and in vitro. Mechanically, the overexpression of MAS1 decreased the expression of PTEN and enhanced the phosphorylation of PI3K and AKT in vivo and in vitro. The overexpression of PTEN and the PI3k inhibitor LY294002 could reverse the MAS1-mediated MI injury. Thus, we conclude that MAS1 inhibits MI-induced myocardial injury by modulating PTEN/PI3K/AKT signaling. Our finding provides new insight into the mechanism by which MAS1 attenuates MI-related cardiac dysfunction.
Keywords: MAS1; MI; Myocardial injury; PTEN/PI3K/AKT signaling.
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