Lu Na, Cheng Weijia, Liu Dongling, Liu Gang, Cui Can, Feng Chaoli, Wang Xianwei
Henan Key Laboratory of Medical Tissue Regeneration, School of Basic Medical Sciences, Xinxiang Medical University, Xinxiang, China.
Department of Cardiology, The First Affiliated Hospital of Xinxiang Medical University, Xinxiang, China.
Front Cell Dev Biol. 2022 Apr 13;10:823387. doi: 10.3389/fcell.2022.823387. eCollection 2022.
The NLRP3 inflammasome is a crucial constituent of the body's innate immune system, and a multiprotein platform which is initiated by pattern recognition receptors (PRRs). Its activation leads to caspase-1 maturation and release of inflammatory cytokines, interleukin-1β (IL-1β) and IL-18, and subsequently causes pyroptosis. Recently, the excess activation of NLRP3 inflammasome has been confirmed to mediate inflammatory responses and to participate in genesis and development of atherosclerosis. Therefore, the progress on the discovery of specific inhibitors against the NLRP3 inflammasome and the upstream and downstream inflammatory factors has become potential targets for clinical treatment. Here we review the recently described mechanisms about the NLRP3 inflammasome activation, and discuss emphatically the pharmacological interventions using statins and natural medication for atherosclerosis associated with NLRP3 inflammasome.
NLRP3炎性小体是机体固有免疫系统的重要组成部分，是由模式识别受体（PRR）启动的多蛋白平台。其激活导致半胱天冬酶-1成熟并释放炎性细胞因子白细胞介素-1β（IL-1β）和IL-18，随后引起细胞焦亡。最近，已证实NLRP3炎性小体的过度激活介导炎症反应并参与动脉粥样硬化的发生和发展。因此，针对NLRP3炎性小体及其上游和下游炎性因子的特异性抑制剂的发现进展已成为临床治疗的潜在靶点。在此，我们综述了最近描述的NLRP3炎性小体激活机制，并着重讨论了使用他汀类药物和天然药物对与NLRP3炎性小体相关的动脉粥样硬化进行的药理干预。
