Chinese PLA General Hospital, Medical School of Chinese PLA, Beijing 100853, China.
Department of Chemical Engineering, University of Minnesota-Duluth, Duluth, MN 55812, USA.
Pharmacol Res. 2020 Jun;156:104771. doi: 10.1016/j.phrs.2020.104771. Epub 2020 Mar 28.
Thrombolytic therapy and revascularization strategies create a complete recanalization of the occluded epicardial coronary artery in patients with myocardial infarction (MI). However, about 35 % of patients still experience an impaired myocardial reperfusion, which is termed a no-reflow phenomenon mainly caused by cardiac microvascular ischemia-reperfusion (I/R) injury. Mitochondria are essential for microvascular endothelial cells' survival, both because of their roles as metabolic energy producers and as regulators of programmed cell death. Mitochondrial structure and function are regulated by a mitochondrial quality control (MQC) system, a series of processes including mitochondrial biogenesis, mitochondrial dynamics/mitophagy, mitochondrial proteostasis, and mitochondria-mediated cell death. Our review discusses the MQC mechanisms and how they are linked to cardiac microvascular I/R injury. Additionally, we will summarize the molecular basis that results in defective MQC mechanisms and present potential therapeutic interventions for improving MQC in cardiac microvascular I/R injury.
溶栓治疗和血运重建策略可使心肌梗死（MI）患者闭塞的心外膜冠状动脉完全再通。然而，约 35%的患者仍存在心肌再灌注受损，这主要是由于心脏微血管缺血再灌注（I/R）损伤引起的无复流现象。线粒体对于微血管内皮细胞的存活至关重要，这是因为它们作为代谢能量产生者和程序性细胞死亡的调节者的作用。线粒体的结构和功能受到线粒体质量控制（MQC）系统的调节，这是一系列包括线粒体生物发生、线粒体动力学/自噬、线粒体蛋白稳态和线粒体介导的细胞死亡的过程。我们的综述讨论了 MQC 机制以及它们与心脏微血管 I/R 损伤的联系。此外，我们将总结导致 MQC 机制缺陷的分子基础，并提出改善心脏微血管 I/R 损伤中 MQC 的潜在治疗干预措施。
