Que Xiangyong, Zheng Sihao, Song Qibin, Pei Huadong, Zhang Pingfeng
Cancer Center, Renmin Hospital of Wuhan University, Wuhan, Hubei 430060, China.
Department of Oncology, Georgetown Lombardi Comprehensive Cancer Center, Georgetown University Medical Center, Washington, DC 20057, USA.
Genes Dis. 2023 Mar 23;11(2):819-829. doi: 10.1016/j.gendis.2023.01.009. eCollection 2024 Mar.
NLRP3 inflammasome, an intracellular multiprotein complex, can be activated by a range of pathogenic microbes or endogenous hazardous chemicals. Its activation results in the release of cytokines such as IL-1β and IL-18, as well as Gasdermin which eventually causes pyroptosis. The activation of NLRP3 inflammasome is under strict control and regulation by numerous pathways and mechanisms. Its excessive activation can lead to a persistent inflammatory response, which is linked to the onset and progression of severe illnesses. Recent studies have revealed that the subcellular localization of NLRP3 changes significantly during the activation process. In this review, we review the current understanding of the molecular mechanism of NLRP3 inflammasome activation, focusing on the subcellular localization of NLRP3 and the associated regulatory mechanisms. We aim to provide a comprehensive understanding of the dynamic transportation, activation, and degradation processes of NLRP3.
NLRP3炎性小体是一种细胞内多蛋白复合物,可被多种致病微生物或内源性有害化学物质激活。其激活会导致细胞因子如IL-1β和IL-18以及Gasdermin的释放,最终导致细胞焦亡。NLRP3炎性小体的激活受到多种途径和机制的严格控制和调节。其过度激活可导致持续性炎症反应,这与严重疾病的发生和发展有关。最近的研究表明,NLRP3在激活过程中的亚细胞定位发生了显著变化。在本综述中,我们回顾了目前对NLRP3炎性小体激活分子机制的理解,重点关注NLRP3的亚细胞定位及相关调节机制。我们旨在全面了解NLRP3的动态运输、激活和降解过程。
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