In conclusion, this present study offers evidence that miR-133a is down-regulated in rats with VMC, and elevated exosomal miR-133a improves cardiac function and restrains myocardial fibrosis and EMT in rats with VMC, as well as enhances viability and represses apoptosis of cardiomyocytes in VMC through targeting MAML1. This evidence concerns the gene MAML1 and Myocardial fibrosis.