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NLRP3 炎性小体通路在动脉粥样硬化中的作用。

NLRP3 inflammasome pathways in atherosclerosis.

机构信息

Department of Medicine, University of Cambridge, The West Forvie Building, Robinson Way, Cambridge, CB2 0SZ, UK.

Department of Medicine, University of Cambridge, The West Forvie Building, Robinson Way, Cambridge, CB2 0SZ, UK; Institut National de la Santé et de la Recherche Médicale, U970, Paris, France.

出版信息

Atherosclerosis. 2017 Dec;267:127-138. doi: 10.1016/j.atherosclerosis.2017.10.027. Epub 2017 Oct 22.

Abstract

Atherosclerosis is the major cause of death and disability. Atherosclerotic plaques are characterized by a chronic sterile inflammation in the large blood vessels, where lipid-derived and damage-associated molecular patterns play important roles in inciting immune responses. Following the initial demonstration that NLR family Pyrin domain containing 3 (NLRP3) was important for atherogenesis, a substantial number of studies have emerged addressing the basic mechanisms of inflammasome activation and their relevance to atherosclerosis. In this review, we introduce the basic cellular and molecular mechanisms of NLRP3 inflammasome activation, and discuss the current findings and therapeutic strategies that target NLRP3 inflammasome activation during the development and progression of atherosclerosis.

摘要

动脉粥样硬化是死亡和残疾的主要原因。动脉粥样硬化斑块的特征是大血管中的慢性非感染性炎症,其中脂质衍生和损伤相关的分子模式在引发免疫反应中起重要作用。最初的研究表明,NLR 家族包含 Pyrin 结构域蛋白 3(NLRP3)对动脉粥样硬化的形成很重要,此后涌现出大量研究,旨在阐明炎性小体激活的基本机制及其与动脉粥样硬化的相关性。在这篇综述中,我们介绍了 NLRP3 炎性小体激活的基本细胞和分子机制,并讨论了针对动脉粥样硬化发生和发展过程中 NLRP3 炎性小体激活的现有研究结果和治疗策略。

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