Shao Bo-Zong, Xu Hai-Yan, Zhao Yi-Cheng, Zheng Xiao-Rui, Wang Fang, Zhao Guan-Ren
Department of Pharmacy, Medical Supplies Center, PLA General Hospital, Beijing, China.
Inflammation. 2023 Feb;46(1):35-46. doi: 10.1007/s10753-022-01725-x. Epub 2022 Aug 11.
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.
动脉粥样硬化（AS）是一种慢性炎症性疾病，其特征为动脉增厚或硬化，导致动脉内膜斑块形成。在所有已阐明的发病机制中，炎症反应过度激活是最被认可的机制之一。核苷酸结合寡聚化结构域样受体蛋白3（NLRP3）炎性小体作为炎症和固有免疫的一种重要且特殊的形式，已被广泛揭示参与动脉粥样硬化的发生和发展。本综述将介绍动脉粥样硬化的发病机制和进展过程，并描述NLRP3炎性小体的生物学特性。此外，还将讨论NLRP3炎性小体在动脉粥样硬化中的作用及可能机制。另外，将详细描述和讨论几种利用NLRP3炎性小体干预发挥抗动脉粥样硬化作用的药物，包括天然化合物（黄芩苷、二氢杨梅素、木犀草素、5-去氧吴茱萸碱（R3）和丹酚酸A等）、微小RNA（微小RNA-30c-5p、微小RNA-9、微小RNA-146a-5p、微小RNA-16-5p和微小RNA-181a等）以及自噬调节剂（褪黑素、膳食多不饱和脂肪酸和阿格拉宾等）。我们旨在为探索动脉粥样硬化的具体机制和开发新的治疗方法提供新的见解。
