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肝脏缺血/再灌注损伤中的线粒体功能障碍与自噬

Mitochondrial Dysfunction and Autophagy in Hepatic Ischemia/Reperfusion Injury.

作者信息

Go Kristina L, Lee Sooyeon, Zendejas Ivan, Behrns Kevin E, Kim Jae-Sung

机构信息

Department of Surgery, University of Florida, Gainesville, FL 32610, USA.

出版信息

Biomed Res Int. 2015;2015:183469. doi: 10.1155/2015/183469. Epub 2015 Dec 6.

Abstract

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.

摘要

缺血/再灌注(I/R)损伤仍然是肝切除、肝移植和失血性休克的主要并发症。尽管导致肝脏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关键事件。线粒体自噬,即所谓的线粒体吞噬,是调节线粒体稳态并及时清除受损线粒体的关键细胞过程。越来越多的证据表明,I/R损伤归因于线粒体自噬缺陷。本综述旨在总结目前对自噬及其在肝脏I/R损伤中的作用的认识,并重点介绍为减轻损伤而研究的各种治疗方法。

https://cdn.ncbi.nlm.nih.gov/pmc/blobs/8ac7/4684839/17e1a74d44ef/BMRI2015-183469.001.jpg

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