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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

  • 摘要: 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(Ca2+)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。

     

    Abstract: 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-1β and IL-18, and regulate imflammatory response.More and more studies in recent years have shown that Ca2+ 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 Ca2+ and NLRP3 inflammasome, focusing on the potential role of Ca2+ signaling in the activation and regulation of NLRP3 inflammasome, to provide new ideas for the treatment of illness caused by NLRP3 inflammasome.

     

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