Liu Chunping, Liu Yanjiao, Chen Huiqi, Yang Xiaofei, Lu Chuanjian, Wang Lei, Lu Jiahong
State Key Laboratory of Quality Research in Chinese Medicine, Institute of Chinese Medical Sciences, University of Macau, Macau, China.
State Key Laboratory of Dampness Syndrome of Chinese Medicine, The Second Affiliated Hospital of Guangzhou University of Chinese Medicine, Guangzhou, 51080, China.
Burns Trauma. 2023 Mar 1;11:tkac062. doi: 10.1093/burnst/tkac062. eCollection 2023.
Autophagy is a highly conserved bulk degradation mechanism that degrades damaged organelles, aged proteins and intracellular contents to maintain the homeostasis of the intracellular microenvironment. Activation of autophagy can be observed during myocardial injury, during which inflammatory responses are strongly triggered. Autophagy can inhibit the inflammatory response and regulate the inflammatory microenvironment by removing invading pathogens and damaged mitochondria. In addition, autophagy may enhance the clearance of apoptotic and necrotic cells to promote the repair of damaged tissue. In this paper, we briefly review the role of autophagy in different cell types in the inflammatory microenvironment of myocardial injury and discuss the molecular mechanism of autophagy in regulating the inflammatory response in a series of myocardial injury conditions, including myocardial ischemia, ischemia/reperfusion injury and sepsis cardiomyopathy.
自噬是一种高度保守的大量降解机制，可降解受损细胞器、老化蛋白质和细胞内成分，以维持细胞内微环境的稳态。在心肌损伤期间可观察到自噬的激活，在此期间会强烈触发炎症反应。自噬可通过清除入侵病原体和受损线粒体来抑制炎症反应并调节炎症微环境。此外，自噬可能会增强凋亡细胞和坏死细胞的清除，以促进受损组织的修复。在本文中，我们简要综述了自噬在心肌损伤炎症微环境中不同细胞类型中的作用，并讨论了自噬在一系列心肌损伤情况（包括心肌缺血、缺血/再灌注损伤和脓毒症心肌病）中调节炎症反应的分子机制。
