Tang Xiaoqu, Fu Xiaoyun, Fu Bao, Liu Xinxin
Department of Critical Care Medicine, Affiliated Hospital of Zunyi Medical University, Zunyi 563000, Guizhou, China. Corresponding author: Fu Xiaoyun, Email:
Zhonghua Wei Zhong Bing Ji Jiu Yi Xue. 2021 Aug;33(8):1007-1010. doi: 10.3760/cma.j.cn121430-20210316-00384.
Mitochondrial unfolded protein response (UPR) is a protein-toxic stress response, which regulates the communication from mitochondria to the nucleus. It is activated when a large number of unfolded or misfolded proteins accumulate in the mitochondria. The activation of UPR increases the expression of a series of chaperones and proteases, and maintains the homeostasis and function of mitochondrial proteins. Mitochondria play an important role in maintaining cardiomyocyte homeostasis. The damage of myocardial mitochondria leads to the metabolic disorder of cells suffering from ischemia/reperfusion injury. It is the key mechanism of myocardial cell death. This article mainly reviews the regulatory pathway of UPR and the research progress of UPR in myocardial ischemia/reperfusion injury (MIRI), in order to provide new ideas for the treatment of MIRI.
线粒体未折叠蛋白反应（UPR）是一种蛋白质毒性应激反应，它调节从线粒体到细胞核的信号传递。当大量未折叠或错误折叠的蛋白质在线粒体中积累时，该反应被激活。UPR的激活会增加一系列分子伴侣和蛋白酶的表达，并维持线粒体蛋白质的稳态和功能。线粒体在维持心肌细胞稳态中起重要作用。心肌线粒体损伤会导致遭受缺血/再灌注损伤的细胞发生代谢紊乱。这是心肌细胞死亡的关键机制。本文主要综述了UPR的调控途径以及UPR在心肌缺血/再灌注损伤（MIRI）中的研究进展，以期为MIRI的治疗提供新思路。
