Current strategies to minimize hepatic ischemia-reperfusion injury by targeting reactive oxygen species

被引:232
作者
Jaeschke, Hartmut [1 ]
Woolbright, Benjamin L. [1 ]
机构
[1] Univ Kansas, Med Ctr, Dept Pharmacol Toxicol & Therapeut, Kansas City, KS 66160 USA
基金
美国国家卫生研究院;
关键词
MITOCHONDRIAL PERMEABILITY TRANSITION; INDUCED LIVER-INJURY; ATRIAL-NATRIURETIC-PEPTIDE; FREE-RADICAL SCAVENGER; PERFUSED RAT-LIVER; NEUTROPHIL NADPH OXIDASE; KUPFFER CELL ACTIVATION; HEAT-SHOCK-PROTEIN; NF-KAPPA-B; ISCHEMIA/REPERFUSION INJURY;
D O I
10.1016/j.trre.2011.10.006
中图分类号
R392 [医学免疫学]; Q939.91 [免疫学];
学科分类号
071005 [微生物学]; 100108 [医学免疫学];
摘要
Ischemia-reperfusion is a major component of injury in vascular occlusion both during liver surgery and during liver transplantation. The pathophysiology of hepatic ischemia-reperfusion includes a number of mechanisms including oxidant stress that contribute to various degrees to the overall organ damage. A large volume of recent research has focused on the use of antioxidants to ameliorate this injury, although results in experimental models have not translated well to the clinic. This review focuses on critical sources and mediators of oxidative stress during hepatic ischemia-reperfusion, the status of current antioxidant interventions, and emerging mechanisms of protection by preconditioning. While recent advances in regulation of antioxidant systems by Nrf2 provide interesting new potential therapeutic targets, an increased focus must be placed on more in-depth mechanistic investigations in hepatic ischemia-reperfusion injury and translational research in order to refine current strategies in disease management. (C) 2012 Elsevier Inc. All rights reserved.
引用
收藏
页码:103 / 114
页数:12
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