肝手术和移植中的缺血/再灌注损伤:病理生理学。

Kilian Weigand, Sylvia Brost, Niels Steinebrunner, Markus Büchler, Peter Schemmer, Martina Müller
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引用次数: 121

摘要

肝脏缺血/再灌注(IR)损伤是由免疫系统细胞、细胞因子产生和肝脏微循环血流减少相互作用的严重齿状网络引起的。这些复杂的网络被细胞因子、趋化因子和危险相关分子模式激活的多种细胞内通路进一步细化。此外,细胞内离子干扰,特别是线粒体紊乱在IR损伤中导致肝细胞凋亡和坏死起重要作用。总的来说,在IR损伤早期发现的活性氧的增强在这些复杂网络中的几个点的肝组织损伤中起着重要作用。到目前为止,许多导致IR损伤的因素还不完全清楚。本文就IR损伤形成的不同机制作一综述。只有进一步阐明这些复杂的IR损伤机制,才有可能改善或开发可能的治疗策略。
本文章由计算机程序翻译,如有差异,请以英文原文为准。

Ischemia/Reperfusion injury in liver surgery and transplantation: pathophysiology.

Ischemia/Reperfusion injury in liver surgery and transplantation: pathophysiology.

Ischemia/Reperfusion injury in liver surgery and transplantation: pathophysiology.

Liver ischemia/reperfusion (IR) injury is caused by a heavily toothed network of interactions of cells of the immune system, cytokine production, and reduced microcirculatory blood flow in the liver. These complex networks are further elaborated by multiple intracellular pathways activated by cytokines, chemokines, and danger-associated molecular patterns. Furthermore, intracellular ionic disturbances and especially mitochondrial disorders play an important role leading to apoptosis and necrosis of hepatocytes in IR injury. Overall, enhanced production of reactive oxygen species, found very early in IR injury, plays an important role in liver tissue damage at several points within these complex networks. Many contributors to IR injury are only incompletely understood so far. This paper tempts to give an overview of the different mechanisms involved in the formation of IR injury. Only by further elucidation of these complex mechanisms IR injury can be understood and possible therapeutic strategies can be improved or be developed.

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