miRNA-145 inhibits myocardial infarction-induced apoptosis through autophagy via Akt3/mTOR signaling pathway in vitr and in vivo

The present study investigated the effects of micro (mi)RNA-145 on acute myocardial infarction (AMI) and the potential underlying mechanism. A total of 6 AMI and 6 normal rat tissues were investigated for the present study. It was demonstrated that miRNA-145 expression was downregulated in the AMI rat model, compared with the control group. Downregulation of miRNA-145 increased cardiac cell apoptosis, suppressed phosphorylated (p)-RAC-γ serine/threonine-protein kinase (Akt3) and p-mechanistic target of rapamycin (mTOR) protein expression levels and suppressed autophagy in an in vitr model of AMI. However, overexpression of miRNA-145 decreased cardiac cell apoptosis, induced p-Akt3 and p-mTOR protein expression and promoted autophagy in the in vitr model of AMI. The inhibition of Akt3 (GSK2110183, 1 nM) decreased the effect of the miRNA-145 upregulation on cell apoptosis in the in vitr model of AMI. Chloroquine diphosphate (5 µM) inhibited the regulatory effect of miRNA-145 upregulation on autophagy to adjust cell apoptosis, in the in vitr model of AMI. The results of the present study demonstrate that miRNA-145 inhibits myocardial infarction-induced apoptosis via autophagy associated with the Akt3/mTOR signaling pathway in viv and in vitro.