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NF-kappaB and reperfusion injury.

机译:NF-κB和再灌注损伤。

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This review discusses the current understanding of mechanisms that mediate activation of the transcription factor nuclear factor-kappaB (NF-kappaB) and how such activation could in turn mediate reperfusion injury. NF-kappaB regulates the expression of several genes involved in inflammation, the immune response, apoptosis, cell survival and proliferation. Many of these same genes are activated during reperfusion injury. The rationale for considering inhibiting NF-kappaB activation as a promising molecular target for ameliorating reperfusion injury in the brain during stroke, the heart during myocardial infarction and the intestines following prolonged ischemia is discussed on the basis of a new understanding of the mechanisms by which NF-kappaB is activated. A complete anthology of the reperfusion injury literature is beyond the scope of this article and the authors apologize to any investigator not cited for their contributions.
机译:这篇综述讨论了目前对介导转录因子核因子-κB(NF-kappaB)激活的机制的理解,以及这种激活又如何介导再灌注损伤。 NF-κB调节与炎症,免疫反应,凋亡,细胞存活和增殖有关的几种基因的表达。这些相同的基因中有许多在再灌注损伤中被激活。在重新认识NF的机制的基础上,讨论了考虑抑制NF-κB活化作为缓解脑卒中,心肌梗塞期间的心脏和长期缺血后的肠道再灌注损伤的有希望的分子靶点的基本原理-kappaB已激活。完整的再灌注损伤文献集不在本文讨论范围之内,作者对未因其贡献而被引用的任何研究者表示歉意。

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