NLRP3炎性小体激活调控机制及抑制剂研究新进展

基础医学与临床 ›› 2020, Vol. 40 ›› Issue (8): 1113-1118.

NLRP3炎性小体激活调控机制及抑制剂研究新进展

周永婷, 叶菜英^*, 朱蕾^*

中国医学科学院基础医学研究所北京协和医学院基础学院药理系, 北京 100005

收稿日期:2020-05-17 修回日期:2020-06-18 出版日期:2020-08-05 发布日期:2020-07-29
通讯作者: ^*caiyingye@126.com; leizhu2004@126.com
基金资助:
国家自然科学基金(81102454); 中国医学科学院医学与健康科技创新工程(2016-I2M-1-002);中国医学科学院医学表观中心基金(2017PT31035, 2018PT31015, 2019PT310017)

New advances in the activation mechanisms of NLRP3 inflammasome and its inhibitors

ZHOU Yong-ting, YE Cai-ying^*, ZHU Lei^*

Department of Pharmacology, Institute of Basic Medical Sciences, Chinese Academy of Medical Sciences, School of Basic Medicine, Peking Union Medical College, Beijing 100005, China

Received:2020-05-17 Revised:2020-06-18 Online:2020-08-05 Published:2020-07-29
Contact: ^*caiyingye@126.com; leizhu2004@126.com

摘要/Abstract

摘要： 含NLR家族PYRIN域蛋白3(NLRP3)炎性小体是一类细胞内多蛋白复合物,可被多种病原微生物或内源性危险分子激活,释放细胞因子IL-1β和IL-18以及引起细胞焦亡,是机体固有免疫的重要组成部分。然而其过度活化可导致慢性炎性反应,与多种重大疾病的发生发展密切相关。因此,深入探究NLRP3炎性小体激活机制对于发展其特异性抑制剂以及相关疾病的治疗具有重要意义。

关键词: NLRP3炎性小体, 活化调控, 抑制剂, 新进展

Abstract: NLRP3 inflammasome is an intracellular multi-protein complex that can be activated by a variety of pathogens and endogenous pathogenic molecules and then leads to the release of cytokines, including interleukin-1β(IL-1β), IL-18 and causes, pyroptosis. It plays an important role in innate immunity. However, the over activation may lead chronic inflammation, which is closely related to the pathogenesis and development of numerous major diseases. Therefore, further investigation on the activation mechanisms of NLRP3 inflammasome is of great significance for the development of its specific inhibitors and the treatment of NLRP3-related diseases.

Key words: NLRP3 inflammasome, activating regulation, inhibitors, new advances

中图分类号:

R967

周永婷, 叶菜英, 朱蕾. NLRP3炎性小体激活调控机制及抑制剂研究新进展[J]. 基础医学与临床, 2020, 40(8): 1113-1118.

ZHOU Yong-ting, YE Cai-ying, ZHU Lei. New advances in the activation mechanisms of NLRP3 inflammasome and its inhibitors[J]. Basic & Clinical Medicine, 2020, 40(8): 1113-1118.

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