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肝脏缺血再灌注损伤:发病机制的现代观点及肝保护的基础——好、坏与致命。

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

机构信息

Australian National University Medical School at the Canberra Hospital, Australian Capital Territory, Australia.

出版信息

J Gastroenterol Hepatol. 2011 Jan;26 Suppl 1:180-7. doi: 10.1111/j.1440-1746.2010.06584.x.

Abstract

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.

摘要

肝缺血再灌注(IR)损伤是肝脏手术和移植中常见的一个重要临床问题。热缺血后再灌注损伤的发病机制复杂,涉及多种不同的细胞类型和固有或动员到肝脏的信号机制。自作者 2003 年在《杂志》上发表综述以来,在增强我们对一些发病途径和肝炎症的关键介质的理解方面取得了相当大的进展,如血红素加氧酶系统、CXC 趋化因子、Toll 样受体以及IR 损伤中实质细胞死亡的模式。更好地了解这些机制将加速设计最佳干预措施以预防肝 IR 损伤和改善肝移植后的结果。

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