Mitochondrial Dysfunction and Autophagy in Hepatic Ischemia/Reperfusion Injury.
Mitochondrial Dysfunction and Autophagy in Hepatic Ischemia/Reperfusion Injury.
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线粒体功能障碍和肝缺血/再灌注损伤中的自噬。
DOI：
10.1155/2015/183469
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发表时间：
2015
影响因子：
--
通讯作者：
Kim JS
中科院分区：
文献类型：
--
作者：
Go KL;Lee S;Zendejas I;Behrns KE;Kim JS
缺血/再灌注(I/R)损伤仍然是肝切除、移植和失血性休克的主要并发症。尽管参与肝脏I/R的机制复杂多样，涉及肝细胞、免疫细胞和内皮细胞损伤的相互作用，但线粒体功能障碍是导致肝脏再灌注损伤的主要事件。线粒体自噬，即所谓的有丝分裂吞噬，是调节线粒体动态平衡和及时消除受损线粒体的关键细胞过程。越来越多的证据表明，I/R损伤可归因于有丝分裂的缺陷。本文就自噬及其在肝脏I/R损伤中的作用的研究现状作一综述，并重点介绍已研究的各种减轻损伤的治疗方法。
Ischemia/reperfusion (I/R) injury remains a major complication of liver resection, transplantation, and hemorrhagic shock. Although the mechanisms that contribute to hepatic I/R are complex and diverse involving the interaction of cell injury in hepatocytes, immune cells, and endothelium, mitochondrial dysfunction is a cardinal event culminating in hepatic reperfusion injury. Mitochondrial autophagy, so-called mitophagy, is a key cellular process that regulates mitochondrial homeostasis and eliminates damaged mitochondria in a timely manner. Growing evidence accumulates that I/R injury is attributed to defective mitophagy. This review aims to summarize the current understanding of autophagy and its role in hepatic I/R injury and highlight the various therapeutic approaches that have been studied to ameliorate injury.