 This study investigates the function and mechanism of MIR 17-5P in myocardial remodelling after myocardial infarction, MI, by using a mouse model of MI and lentivirus antigo, MIR 17-5P vector. The results show that inhibition of MIR 17-5P expression can improve myocardial fibrosis, scarring, and cardiomyocid apoptosis decrease LC3-2-LC3 eye ratio and becklin-1 but increase P62 expression. The dual-leuciferase assay suggests that MIR 17-5P target STAT 3 and negatively regulates its expression. Inhibition of STAT 3 expression using S31-201 can deteriorate the improvement of myocardial remodelling, along with the rise of LC3-2-LC3 eye and becklin-1 expression, the reduction of P62 expression and the reversion of MI attenuation. In conclusion, inhibition of MIR 17-5P can inhibit myocardial autophagy through targeting STAT 3 and then inhibit myocardial remodelling, thereby protecting the myocardium after MI. This article was authored by Bo Chen, Ying Zhenyang, Jingbo Wu, and others. We are article.tv, links in the description below.