钙离子信号介导Nod样受体蛋白炎性小体激活的研究进展

Calcium signal-mediated activation of NLRP3 inflammasome

Nod样受体蛋白(Nod-like receptor protein 3,NLRP3)炎性小体可识别多种病原体及细胞损伤,诱导分泌白细胞介素1β(interleukin-1β,IL-1β)、IL-18,调节炎症反应,是固有免疫系统的重要组成部分。近年研究表明,钙离子(Ca^(2+))信号参与多种NLRP3激动剂诱导的NLRP3炎性小体激活过程,并与相关疾病的发生密切相关。本文综述了有关钙离子与NLRP3炎性小体的相关研究,重点关注钙离子信号在NLRP3炎性小体激活和调节中的潜在作用,为治疗NLRP3炎性小体驱动的炎症性疾病提供新思路。

Nod-like receptor protein 3(NLRP3)inflammasome,which is an important component of the innate immune system,can recognize a variety of pathogens and cell damage,induce the secretion of IL-1βand IL-18,and regulate imflammatory response.More and more studies in recent years have shown that Ca^(2+) signaling plays an important role in NLRP3 inflammasome activation induced by various NLRP3 inflammasome agonists,and is closely related to the occurrence of related diseases.The article reviews the literatures on Ca^(2+) and NLRP3 inflammasome,focusing on the potential role of Ca^(2+) signaling in the activation and regulation of NLRP3 inflammasome,to provide new ideas for the treatment of illness caused by NLRP3 inflammasome.