ITGB1 Alleviates High Glucose-Induced Myocardial Cell Injury by Inhibiting Endoplasmic Reticulum Stress and Cell Apoptosis.

Abstract

Diabetic cardiopathy is a common clinical complication of diabetes and is one of the main causes of mortality in type 2 diabetes mellitus patients. In this study, we examined the effect and mechanism of integrin β1 (ITGB1) on high glucose-induced myocardial cell injury. High glucose exposure inhibits the expression of ITGB1 in myocardial cells. ITGB1 inhibited the apoptosis and growth inhibition induced by high glucose. Additionally, the high glucose-induced expression of HSPA5, IRE1α, XBP1, CHOP, ATF6, and cleaved-caspase12 was downregulated significantly when ITGB1 was overexpressed in the presence of high glucose, showing that ITGB1 alleviated endoplasmic reticulum (ER) stress triggered by high glucose. Mechanistically, ITGB1 activated the FAK/ERK singling pathway in high glucose-treated myocardial cells. In the rescue experiment conducted using a signaling pathway inhibitor, overexpression of ITGB1 could not alleviate the effect of high glucose on cell activity and apoptosis in the presence of an inhibitor. In conclusion, ITGB1 alleviates high glucose-induced myocardial cell injury by activating the FAK/ERK singling pathway in myocardial cells. This research contributed to the understanding of the pathogenesis of diabetic cardiopathy and the development of novel drugs and therapeutic targets for it.