NLRP3 inflammasome pathways in atherosclerosis

被引：161

作者：

Baldrighi, Marta ^{[1
]}

Mallat, Ziad ^{[1
,2
]}

Li, Xuan ^{[1
]}

机构：

[1] Univ Cambridge, Dept Med, West Forvie Bldg,Robinson Way, Cambridge CB2 0SZ, England

[2] INSERM, U970, Paris, France

来源：

ATHEROSCLEROSIS | 2017年 / 267卷

关键词：

Atherosclerosis; NLRP3; inflammasome; ASC; Caspase-1; IL-1; beta; ENDOPLASMIC-RETICULUM STRESS; NALP3; INFLAMMASOME; CHOLESTEROL CRYSTALS; CLONAL HEMATOPOIESIS; BINDING-PROTEIN; K+ EFFLUX; ACTIVATION; EXPRESSION; DEFICIENCY; RELEASE;

D O I：

10.1016/j.atherosclerosis.2017.10.027

中图分类号：

R5 [内科学];

学科分类号：

100201 [内科学];

摘要：

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. Crown Copyright (C) 2017 Published by Elsevier Ireland Ltd.

引用

页码：127 / 138

页数：12

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