Key result
Inhibition of miR-17-5p protected the myocardium after myocardial infarction by inhibiting myocardial autophagy and remodelling through the targeting of STAT3.
Why the study?
MicroRNAs regulate myocardial infarction, but the function and mechanism of miR-17-5p in myocardial remodelling after myocardial infarction required investigation.
Does inhibition of miR-17-5p improve myocardial remodeling after myocardial infarction in a mouse model?
Does inhibition of miR-17-5p improve myocardial remodeling after myocardial infarction in a mouse model?
Inhibition of miR-17-5p protects against myocardial remodeling and autophagy after myocardial infarction by targeting STAT3 in a mouse model.
Inhibition of miR-17-5p attenuates post-MI remodeling in mice; leaves open therapeutic translation and requires human validation.
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.
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Chen et al. (2021) studied Myocardial infarction. Lentivirus antago-miR-17-5p vector was evaluated on Myocardial fibrosis, scarring, cardiomyocyte apoptosis, and autophagy markers. Inhibition of miR-17-5p protected the myocardium after myocardial infarction by inhibiting myocardial autophagy and remodelling through the targeting of STAT3.
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