Department of Cardiology and Shanghai Institute of Cardiovascular Diseases, Zhongshan Hospital, Fudan University, Shanghai 200032, PR China.
School of Pharmacy, University of Wyoming College of Health Sciences, Laramie, WY 82071, USA.
Biochim Biophys Acta Mol Basis Dis. 2019 Sep 1;1865(9):2293-2302. doi: 10.1016/j.bbadis.2019.05.007. Epub 2019 May 14.
Ischemia-reperfusion injury (IR injury), produced by initial interruption and subsequent restoration of organ blood flow, is an important clinical dilemma accompanied by various cardiac reperfusion strategies following acute myocardial infarction (AMI). Although the restored blood flow is necessary for oxygen and nutrient supply, reperfusion often results in pathological sequelae leading to elevated ischemic damage. Among various theories postulated for IR injury including vascular leakage, oxidative stress, leukocyte entrapment, inflammation and apoptosis, mitochondrial dysfunction plays an essential role in mediating pathophysiological processes with recent evidence depicting a pivotal role for impaired mitophagy in mitochondrial injury. Given the critical role for mitophagy in mitochondrial quality control and the recent reports supporting a tie between mitophagy and IR injury, this review will revisit the contemporary understanding of mitophagy in the regulation of cardiac homeostasis and update recent progresses with regards to mitophagy and cardiac IR injury. We hope to establish a role for mitophagy as a potential therapeutic target in the management of IR injury.
缺血再灌注损伤（IR 损伤）是由器官血流最初中断和随后恢复引起的，是急性心肌梗死（AMI）后各种心脏再灌注策略所伴随的一个重要临床难题。尽管恢复血流对于氧和营养物质的供应是必要的，但再灌注通常会导致病理后果，导致缺血性损伤增加。在包括血管渗漏、氧化应激、白细胞捕获、炎症和细胞凋亡在内的各种 IR 损伤理论中，线粒体功能障碍在介导病理生理过程中起着至关重要的作用，最近的证据表明，受损的线粒体自噬在线粒体损伤中起着关键作用。鉴于线粒体自噬在调节线粒体质量控制中的关键作用，以及最近关于线粒体自噬与 IR 损伤之间联系的报道，本综述将重新审视线粒体自噬在心脏稳态调节中的现代认识，并更新关于线粒体自噬和心脏 IR 损伤的最新进展。我们希望确定线粒体自噬作为 IR 损伤管理中潜在治疗靶点的作用。
