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Erschienen in: Inflammation 1/2023

11.08.2022 | Review

NLRP3 Inflammasome in Atherosclerosis: Putting Out the Fire of Inflammation

verfasst von: Bo-Zong Shao, Hai-Yan Xu, Yi-Cheng Zhao, Xiao-Rui Zheng, Fang Wang, Guan-Ren Zhao

Erschienen in: Inflammation | Ausgabe 1/2023

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Abstract

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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Metadaten
Titel
NLRP3 Inflammasome in Atherosclerosis: Putting Out the Fire of Inflammation
verfasst von
Bo-Zong Shao
Hai-Yan Xu
Yi-Cheng Zhao
Xiao-Rui Zheng
Fang Wang
Guan-Ren Zhao
Publikationsdatum
11.08.2022
Verlag
Springer US
Erschienen in
Inflammation / Ausgabe 1/2023
Print ISSN: 0360-3997
Elektronische ISSN: 1573-2576
DOI
https://doi.org/10.1007/s10753-022-01725-x

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