论文部分内容阅读
Myocardial injury is still a serious condition damaging the public health.Clinically,myocardial injury often leads to cardiac dysfunction and,in severe cases,death.Reperfusion of the ischemic myocardial tissues can minimize acute myocardial infarction(AMI)-induced damage.MicroRNAs are commonly recognized in diverse diseases and are often involved in the development of myocar-dial ischemia/reperfusion injury.However,the role of miR-431 remains unclear in myocardial injury.In this study,we investigated the underlying mechanisms of miR-431 in the cell apoptosis and autophagy of human cardiomyocytes in hypoxia/reoxygenation(H/R).H/R treatment reduced cell viability,promoted cell apoptotic rate,and down-regulated the expression of miR-431 in human cardiomyocytes.The down-regulation of miR-431 by its inhibitor reduced cell viability and induced cell apoptosis in the human cardiomyocytes.Moreover,miR-431 down-regulated the expression of autophagy-related 3(ATG3)via targeting the 3'-untranslated region of ATG3.Up-regulated expres-sion of ATG3 by pcDNA3.1-ATG3 reversed the protective role of the overexpression of miR-431 on cell viability and cell apoptosis in H/R-treated human cardiomyocytes.More importantly,H/R treat-ments promoted autophagy in the human cardiomyocytes,and this effect was greatly alleviated via miR-431-mimic transfection.Our results suggested that miR-431 overexpression attenuated the H/R-induced myocardial damage at least partly through regulating the expression of ATG3.