Hepatic ischemia reperfusion injury: Contemporary perspectives on pathogenic mechanisms and basis for hepatoprotection-the good, bad and deadly

被引:76
作者
Teoh, Narci C. [1 ]
机构
[1] Australian Natl Univ, Gastroenterol & Hepatol Unit, Sch Med, Canberra Hosp, Garran, ACT 2605, Australia
关键词
chemokines; heme oxygenase; hepatocyte cell death; Inflammation; kupffer cells; liver ischemia reperfusion injury; neutrophils; Receptor for Advanced Glycation End Products (RAGE); Toll-Like Receptor (TLR); tumor necrosis factor-alpha; NECROSIS-FACTOR-ALPHA; TOLL-LIKE RECEPTOR; HEME OXYGENASE SYSTEM; ISCHEMIA/REPERFUSION INJURY; LIVER-INJURY; IN-VIVO; INFLAMMATORY RESPONSE; BILIVERDIN REDUCTASE; REOXYGENATION INJURY; XANTHINE-OXIDASE;
D O I
10.1111/j.1440-1746.2010.06584.x
中图分类号
R57 [消化系及腹部疾病];
学科分类号
摘要
Hepatic ischemia reperfusion (IR) injury is an important clinical problem complicating liver surgery and transplantation. The pathogenesis underlying reperfusion injury after warm ischemia is complex, encompassing a multitude of different cell types and signalling mechanisms innate and/or mobilized to the liver. Since the author's 2003 review in the Journal, considerable progress has been achieved in enhancing our understanding of some of the pathogenic pathways and crucial mediators of hepatic inflammation such as the heme oxygenase system, CXC chemokines, Toll-like receptors as well as the mode of parenchymal cell death in IR injury. A better appreciation of these mechanisms will accelerate efforts in designing optimal interventions to prevent hepatic IR injury and improve outcomes after liver transplantation.
引用
收藏
页码:180 / 187
页数:8
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