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Past and future approaches to ischemia-reperfusion lesion associated with liver transplantation

机译：肝移植相关缺血再灌注病变的过去和未来方法

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摘要

Ischemia-reperfusion (I/R) injury associated with liver transplantation remains a serious complication in clinical practice, in spite of several attempts to solve the problem. The present review focuses on the complexity of I/R injury, summarizing conflicting results obtained from the literature about the mechanisms responsible for it. We also review the therapeutic strategies designed in past years to reduce UR injury, attempting to explain why most of them have not been applied clinically These strategies include improvements in phannacological treatments, modifications of University of Wisconsin (UW) preservation solution based on a variety of additives, and gene therapy. Finally, we will consider new potential protective strategies using trimetazidine, 5-amino-4-imidazole carboxamide riboside (AICAR), melatonin, modulators of the renin-angiotensin system (RAS) and the phosphatidylinositol-3-OH kinase (PI3K)-Akt and the p42/p44 extracellular signal-regulated kinases (Erk 1/2) pathway. These strategies have shown promising results for UR injury but have not been tested in experimental liver transplantation to date. Moreover, we will review ischemic preconditioning, taking into account the recent clinical studies that suggest that this surgical strategy could be appropriate for liver transplantation. (c) 2006 Elsevier Inc. All rights reserved.
机译：尽管进行了多次尝试来解决与肝脏移植相关的缺血再灌注（I / R）损伤，但在临床实践中仍然是一个严重的并发症。本综述着重于I / R损伤的复杂性，总结了从文献中获得的有关引起I / R损伤的机制的矛盾结果。我们还回顾了过去几年中为减轻UR损伤而设计的治疗策​​略，试图解释为何大多数方法尚未在临床上应用。这些策略包括药理学治疗方法的改进，威斯康星大学（UW）防腐溶液的改良，基于多种添加剂和基因疗法。最后，我们将考虑使用曲美他嗪，5-氨基-4-咪唑羧酰胺核糖苷（AICAR），褪黑激素，肾素-血管紧张素系统的调节剂（RAS）和磷脂酰肌醇-3-OH激酶（PI3K）-Akt的新的潜在保护策略和p42 / p44细胞外信号调节激酶（Erk 1/2）途径。这些策略已显示出对UR损伤有希望的结果，但迄今为止尚未在实验性肝移植中进行测试。此外，我们将回顾缺血性预处理，同时考虑到最近的临床研究表明该手术策略可能适合于肝移植。 （c）2006 Elsevier Inc.保留所有权利。

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