ETV1 and myocardial infarction: Our previous study demonstrated that ETV1 is a potential transcription factor involved in regulating gene expression and ventricular remodeling after AMI; In this study, we found that the expression of ETV1 was downregulated after MI, and endothelial-specific overexpression of ETV1 mitigated the deterioration of cardiac function, inhibited myocardial apoptosis and fibrosis, and promoted angiogenesis after MI; in vitro experiments showed that overexpression of ETV1 promotes the migration and tube formation of HUVECs.