Department of Cardiology, Dongfang Hospital, the Second Affiliated Hospital of Beijing University of Chinese Medicine, Beijing, 100078, China.
Department of Cardiology, Dongzhimen Hospital, the First Affiliated Hospital of Beijing University of Chinese Medicine, Beijing, 100007, China.
Chin J Integr Med. 2023 Jan;29(1):81-88. doi: 10.1007/s11655-021-3301-1. Epub 2021 Nov 3.
Mitophagy is one of the important targets for the prevention and treatment of myocardial ischemia/reperfusion injury (MIRI). Moderate mitophagy can remove damaged mitochondria, inhibit excessive reactive oxygen species accumulation, and protect mitochondria from damage. However, excessive enhancement of mitophagy greatly reduces adenosine triphosphate production and energy supply for cell survival, and aggravates cell death. How dysfunctional mitochondria are selectively recognized and engulfed is related to the interaction of adaptors on the mitochondrial membrane, which mainly include phosphatase and tensin homolog deleted on chromosome ten (PTEN)-induced kinase 1/Parkin, hypoxia-inducible factor-1 α/Bcl-2 and adenovirus e1b19k Da interacting protein 3, FUN-14 domain containing protein 1 receptor-mediated mitophagy pathway and so on. In this review, the authors briefly summarize the main pathways currently studied on mitophagy and the relationship between mitophagy and MIRI, and incorporate and analyze research data on prevention and treatment of MIRI with Chinese medicine, thereby provide relevant theoretical basis and treatment ideas for clinical prevention of MIRI.
自噬是防治心肌缺血再灌注损伤（MIRI）的重要靶点之一。适度的自噬可以清除受损的线粒体，抑制过多的活性氧积累，从而保护线粒体免受损伤。然而，过度增强的自噬会大大降低细胞生存所需的三磷酸腺苷的产生和能量供应，加重细胞死亡。功能失调的线粒体如何被选择性识别和吞噬与线粒体膜上衔接蛋白的相互作用有关，主要包括磷酸酶和张力蛋白同源物缺失的第十染色体（PTEN）诱导激酶 1/ Parkin、低氧诱导因子-1α/Bcl-2 和腺病毒 e1b19kDa 相互作用蛋白 3、FUN-14 结构域包含蛋白 1 受体介导的自噬途径等。本文作者简要总结了目前研究自噬的主要途径及其与 MIRI 的关系，并整合和分析了中药防治 MIRI 的研究数据，从而为临床预防 MIRI 提供了相关的理论依据和治疗思路。
