microRNA-17-5p downregulation inhibits autophagy and myocardial remodelling after myocardial infarction by targeting STAT3

MicroRNAs (miRs) are reported to regulate myocardial infarction (MI). This study was performed to investigate the function and mechanism of miR-17-5p in myocardial remodelling after MI. Initially, a mouse model of MI was established and MI mice were infected with lentivirus antago-miR-17-5p vector. High expression of miR-17-5p was found in myocardial tissues after MI. After inhibiting miR-17-5p expression, myocardial fibrosis, scarring, and cardiomyocyte apoptosis were improved, LC3-II/LC3-I ratio and Beclin-1 expression were decreased but p62 expression was increased. The dual-luciferase assay suggested that miR-17-5p targeted STAT3 and negatively regulated its expression. Then, after inhibiting STAT3 expression using STAT3 inhibitor S31-201, the fibrosis, scarring, and cardiomyocyte apoptosis were deteriorated, along with the rise of LC3-II/LC3-I and Beclin-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 STAT3 and then inhibit myocardial remodelling, thereby protecting the myocardium after MI.

Automated summary

miR-17-5p regulates myocardial remodeling after myocardial infarction by targeting STAT3, leading to protection of the myocardium. Inhibiting the expression of miR-17-5p can alleviate myocardial fibrosis and cardiomyocyte apoptosis.