氧调节蛋白150与糖尿病心肌缺血/再灌注损伤关系的研究进展

Research Progress of Relationship between Oxygen-Regulated Protein 150 and Diabetic Myocardial Ischemia/Reperfusion Injury

病理过程持续存在或加重可破坏内质网内稳态引起内质网应激(ERS)。ERS在高糖高脂、缺血缺氧、钙平衡紊乱等病理情况中发挥重要作用。在糖尿病心肌缺血/再灌注损伤过程中,ERS及其随后发生的非折叠蛋白反应引起的心肌细胞的凋亡加重这一病理过程。实验表明,氧调节蛋白150(ORP150)的过表达可减轻ERS引起的心肌细胞的凋亡,进而减轻糖尿病心肌损伤。本文就ORP150通过对ERS的作用,进而对糖尿病心肌缺血/再灌注损伤中的作用进行了介绍,为糖尿病缺血/再灌注的心肌治疗提供科学依据。

Persist or worsen the pathological process, such as hyperglycemia and hyperlipidemia, ischemia and hypoxia , and calcium balance disorders, can destroy the endoplasmic reticulum homeostasis cause endoplasmic reticulum stress （ERS）. ERS plays an important role in pathological conditions. In the course of diabetic myocardial ischemia-reperfusion injury, the pathological process is aggravated by apoptosis of cardiomyocytes caused by ERS and its subsequent unfolded protein reaction. Experiments have shown that overexpression of oxygen-regulated protein 150 （ORP150） can reduce the apoptosis of cardiomyocytes induced by ERS, thereby reducing myocardial injury in diabetic rats. This article describes the role of ORP150 in ERS for diabetic myocardial ischemia-reperfusion injury, providing a scientific basis for the treatment of diabetic myocardial ischemia and reperfusion.