Li Yi, Wu Hui, Zhang Songlin, Zhou Gang, Zhang Dong, Yang Qingzhuo, Liu Yanfang, Huang Xiaoli
Institute of Cardiovascular disease, China Three Gorges University, 443003 Yichang, Hubei, China.
Department of Thoracic and Cardiac Surgery, Yichang Central People's Hospital, 443003 Yichang, Hubei, China.
Rev Cardiovasc Med. 2024 Mar 26;25(4):113. doi: 10.31083/j.rcm2504113. eCollection 2024 Apr.
In recent years, the interaction of intracellular organelles such as mitochondria and lysosomal functions has attracted increasing attention. Recent evidence suggests that mitochondrion-lysosomal contact plays a key role in regulating lysosomal biogenesis and maintaining cellular homeostasis. Myocardial ischemia and reperfusion will lead to corresponding changes in the autophagy flux in cardiomyocytes, and lysosomes are a key link in the process of autophagy, and the fusion of lysosomes and autophagosomes is an essential link in the occurrence of autophagy. Therefore, the function and homeostasis of lysosomes also undergo different changes during myocardial ischemia and reperfusion. Lysosomal-related biological factors and membrane proteins also play different roles. This article will review the mechanism of lysosomes in myocardial ischemia-reperfusion injury and the research progress of lysosomal-related proteins.
近年来，线粒体等细胞内细胞器与溶酶体功能的相互作用日益受到关注。最近的证据表明，线粒体-溶酶体接触在调节溶酶体生物发生和维持细胞内稳态中起关键作用。心肌缺血再灌注会导致心肌细胞自噬通量发生相应变化，而溶酶体是自噬过程中的关键环节，溶酶体与自噬体的融合是自噬发生的必要环节。因此，溶酶体的功能和内稳态在心肌缺血再灌注过程中也会发生不同变化。溶酶体相关生物因子和膜蛋白也发挥着不同作用。本文将综述溶酶体在心肌缺血再灌注损伤中的机制以及溶酶体相关蛋白的研究进展。
