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炎症小体、细胞焦亡与心肌缺血再灌注损伤中的细胞因子。

Inflammasome, pyroptosis, and cytokines in myocardial ischemia-reperfusion injury.

机构信息

VCU Pauley Heart Center , Richmond, Virginia.

VCU Johnson Center for Critical Care and Pulmonary Research , Richmond, Virginia.

出版信息

Am J Physiol Heart Circ Physiol. 2018 Dec 1;315(6):H1553-H1568. doi: 10.1152/ajpheart.00158.2018. Epub 2018 Aug 31.

Abstract

Myocardial ischemia-reperfusion injury induces a sterile inflammatory response, leading to further injury that contributes to the final infarct size. Locally released danger-associated molecular patterns lead to priming and triggering of the NOD-like receptor protein 3 inflammasome and amplification of the inflammatory response and cell death by activation of caspase-1. We review strategies inhibiting priming, triggering, or caspase-1 activity or blockade of the inflammasome-related cytokines interleukin-1β and interleukin-18, focusing on the beneficial effects in experimental models of acute myocardial infarction in animals and the initial results of clinical translational research trials.

摘要

心肌缺血再灌注损伤会引起无菌性炎症反应,导致进一步的损伤,进而影响梗死面积。局部释放的危险相关分子模式会导致 NOD 样受体蛋白 3 炎性小体的激活和放大炎症反应和细胞死亡,从而导致 caspase-1 的激活。我们综述了抑制心肌缺血再灌注损伤的策略,包括抑制 NOD 样受体蛋白 3 炎性小体的激活和放大炎症反应和细胞死亡的 caspase-1 活性,以及阻断炎性小体相关细胞因子白细胞介素-1β和白细胞介素-18 的作用,重点介绍了在动物急性心肌梗死模型中的有益作用和临床转化研究试验的初步结果。

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