Abstract
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 vitro 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 vitro model of AMI. The inhibition of Akt3 (GSK2110183, 1 nM) decreased the effect of the miRNA‑145 upregulation on cell apoptosis in the in vitro model of AMI. Chloroquine diphosphate (5 µM) inhibited the regulatory effect of miRNA‑145 upregulation on autophagy to adjust cell apoptosis, in the in vitro 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 vivo and in vitro.