However, in an acute myocardial infarction model, it has been reported that the mechanisms by which miR-145 improves the cardiac function involving acceleration of autophagy of cardiomyocytes through targeting fibroblast growth factor receptor substrate 2 (FRS2) [13], and that the mechanism by which miR-143 improves cardiac function is through decreasing oxidative stress that causes autophagy cell death by silencing COX-1, COX-2 and ATG7 [14]. This evidence concerns the gene ATG7 and myocardial infarction.