Autophagy and liver ischemia-reperfusion injury.

Autophagy and liver ischemia-reperfusion injury.
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DOI:
10.1155/2015/417590
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发表时间:
2015
影响因子:
--
通讯作者:
Gugenheim J
Gugenheim J
中科院分区:
生物学3区
文献类型:
--
作者:
Cursio R;Colosetti P;Gugenheim J

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肝缺血再灌注损伤发生在肝切除、肝移植和失血性休克过程中。热和/或冷肝I-R后肝细胞死亡的主要模式是坏死,但也涉及其他细胞死亡模式,如凋亡和自噬。自噬是一种细胞内的自我消化途径,负责清除溶酶体生物合成过程中的长寿命蛋白质、受损细胞器和畸形蛋白质。自噬存在于正常和病变的肝脏中。虽然取决于缺血的类型,温暖和/或寒冷,肝脏I-R的动态过程主要导致三磷酸腺苷消耗和活性氧(ROS)的产生,导致局部缺血损伤和急性炎症介导的再灌注损伤,并最终导致细胞死亡。这一过程可引起肝功能障碍,并可增加肝脏手术和失血性休克后患者的发病率和死亡率。自噬是否保护或促进热和/或冷I-R后的肝损伤仍有待阐明。本文综述了目前对肝缺血再灌注损伤的认识,重点介绍了热和/或冷肝缺血再灌注后肝自噬的有益和有害作用。
Liver ischemia-reperfusion (I-R) injury occurs during liver resection, liver transplantation, and hemorrhagic shock. The main mode of liver cell death after warm and/or cold liver I-R is necrosis, but other modes of cell death, as apoptosis and autophagy, are also involved. Autophagy is an intracellular self-digesting pathway responsible for removal of long-lived proteins, damaged organelles, and malformed proteins during biosynthesis by lysosomes. Autophagy is found in normal and diseased liver. Although depending on the type of ischemia, warm and/or cold, the dynamic process of liver I-R results mainly in adenosine triphosphate depletion and in production of reactive oxygen species (ROS), leads to both, a local ischemic insult and an acute inflammatory-mediated reperfusion injury, and results finally in cell death. This process can induce liver dysfunction and can increase patient morbidity and mortality after liver surgery and hemorrhagic shock. Whether autophagy protects from or promotes liver injury following warm and/or cold I-R remains to be elucidated. The present review aims to summarize the current knowledge in liver I-R injury focusing on both the beneficial and the detrimental effects of liver autophagy following warm and/or cold liver I-R.
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