Hepatic ischemia/reperfusion injury - a fresh look
Hepatic ischemia/reperfusion injury - a fresh look
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DOI：
10.1016/s0014-4800(03)00008-x
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发表时间：
2003-04-01
影响因子：
3.6
通讯作者：
Kupiec-Weglinski, JW
中科院分区：
文献类型：
--
作者：
Fondevilla, C;Busuttil, RW;Kupiec-Weglinski, JW
肝移植后缺血再灌注（I/R）损伤是影响移植物功能的多因素过程。了解I/R损伤的机制对于设计改善肝移植预后的治疗策略至关重要。再氧化后活性氧的产生会造成组织损伤，并引发一系列有害的细胞反应，导致炎症、细胞死亡和最终的器官衰竭。越来越多的实验证据表明，Kupffer细胞和T细胞介导中性粒细胞炎症反应的激活。活化的中性粒细胞浸润损伤的肝脏，同时内皮细胞粘附分子表达增加。血红素加氧酶系统是细胞应激时激活的细胞保护机制中最关键的一个，发挥抗氧化和抗炎功能，调节细胞周期，维持微循环。最后，基于肝I/R损伤代表宿主“先天”免疫的概念，库普弗细胞上toll样受体的激活可能在探索新的治疗策略中发挥重要作用。(C) 2003 Elsevier Science（美国）版权所有。
Ischemia/reperfusion (I/R) injury is a multifactorial process that affects graft function after liver transplantation. An understanding of the mechanisms involved in I/R injury is essential for the design of therapeutic strategies to improve the outcome of liver transplantation. The generation of reactive oxygen species subsequent to reoxygenation inflicts tissue damage and initiates a cascade of deleterious cellular responses leading to inflammation, cell death, and ultimate organ failure. Increased experimental evidence has suggested that Kupffer cells and T cells mediate the activation of neutrophil inflammatory responses. Activated neutrophils infiltrate the injured liver in parallel with increased expression of adhesion molecules on endothelial cells. The heme oxygenase system is among the most critical of the cytoprotective mechanisms activated during cellular stress, exerting antioxidant and anti-inflammatory functions, modulating the cell cycle, and maintaining the microcirculation. Finally, the activation of toll-like receptors on Kupffer cells may play a fundamental role in exploring new therapeutic strategies based on the concept that hepatic I/R injury represents a case for a host "innate" immunity. (C) 2003 Elsevier Science (USA). All rights reserved.