NLRP3 Inflammasome in Atherosclerosis: Putting Out the Fire of Inflammation

炎症体 吡喃结构域 炎症 NALP3 发病机制 小RNA 先天免疫系统 免疫学 医学 细胞生物学 生物 免疫系统 生物化学 基因
作者
Bo‐Zong Shao,Haiyan Xu,Yicheng Zhao,Xiao-Rui Zheng,Fang Wang,Guan-Ren Zhao
出处
期刊:Inflammation [Springer Science+Business Media]
卷期号:46 (1): 35-46 被引量:26
标识
DOI:10.1007/s10753-022-01725-x
摘要

Atherosclerosis (AS) is a chronic inflammatory disease with thickening or hardening of the arteries, which led to the built-up of plaques in the inner lining of an artery. Among all the clarified pathogenesis, the over-activation of inflammatory reaction is one of the most acknowledged one. The nucleotide-binding domain leucine-rich repeat (NLR) and pyrin domain containing receptor 3 (NLRP3) inflammasome, as a vital and special form of inflammation and innate immunity, has been widely revealed to participate in the onset and development of AS. This review will introduce the process of the pathogenesis and progression of AS, and will describe the biological features of the NLRP3 inflammasome. Furthermore, the role of the NLRP3 inflammasome in AS and the possible mechanisms will be discussed. In addition, several kinds of agents with the effect of anti-atherosclerotic taking advantage of the NLRP3 inflammasome intervention will be described and discussed in detail, including natural compounds (baicalin, dihydromyricetin, luteolin, 5-deoxy-rutaecarpine (R3) and Salvianolic acid A, etc.), microRNAs (microRNA-30c-5p, microRNA-9, microRNA-146a-5p, microRNA-16-5p and microRNA-181a, etc.), and autophagy regulators (melatonin, dietary PUFA and arglabin, etc.). We aim to provide novel insights in the exploration of the specific mechanisms of AS and the development of new treatments of AS.
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