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

• DOI: 10.23736/s0031-0808.20.03979-8
• Publication Date: 2021-09-14T08:03:11Z
• Authors: Shilin TANG; Yang WANG; Tanya MA; Shijuan LU; Kang HUANG; Qiang LI; Miao WU; Hui YANG; Jianghua ZHONG
• Keywords: GPX4

BACKGROUND: To investigate the effect of microRNA-30d (miR-30d) on autophagy and reveal mechanism promoting ferroptosis in H9C2 cells.METHODS: First, we detected miR-30d expression myocardial tissue sham infarction (MI) group, then analyzed by biochemical analysis luciferase Genetic experiments to confirm its downstream target gene of. After using Lentivirus-ATG5 (LV-sh-ATG5) effectively inhibit autophagy, order further clarify possible leading cells, have tested relevant indicators ferroptosis.RESULTS: We first found that was down-regulated after MI, while increased, reduced when overexpressed, confirmed ATG5 a miR-30d. (LV-shATG5) up-regulate FTH1 GPX4 reduce content MDA, increase GSH, activity GPX4, suggesting MI may promote cells.CONCLUSIONS: The decreased cardiomyocytes which can binding ATG5. Furthermore, ferroptosis.