MiR-30d inhibits cardiomyocytes autophagy promoting ferroptosis after myocardial infarction.

BACKGROUND

The aim of this study was to investigate the effect of microRNA-30d (miR-30d) on autophagy and reveal the mechanism of autophagy promoting ferroptosis in H9C2 cells.

METHODS

First, we detected miR-30d expression of myocardial tissue in the sham and myocardial infarction (MI) group, and then analyzed by biochemical analysis and luciferase Genetic experiments to confirm its downstream target gene of. After using Lentivirus-ATG5 (LV-sh-ATG5) to effectively inhibit autophagy, in order to further clarify the possible mechanism of autophagy leading to ferroptosis in H9C2 cells, we have tested the relevant indicators ferroptosis.

RESULTS

We first found that miR-30d expression was down-regulated in myocardial tissue after MI, while autophagy increased, and autophagy was reduced when miR-30d was overexpressed, and then analyzed by biochemical analysis and luciferase Genetic experiments confirmed that ATG5 was a downstream target gene of miR-30d. After using Lentivirus-ATG5 (LV-shATG5) to effectively inhibit autophagy and up-regulate the expression of FTH1 and GSH peroxidase (GPX4) in H9C2 cells, reduce the content of MDA, increase the content of GSH, and increase the activity of GPX4, suggesting that autophagy after MI may promote ferroptosis in H9C2 cells.

CONCLUSIONS

The expression of miR-30d decreased in cardiomyocytes after MI and which can inhibit autophagy by binding to ATG5. Furthermore, autophagy after MI may promote ferroptosis.