%0 Journal Article
%T Recent advances in the mechanisms of NLRP3 inflammasome activation and its inhibitors
%A Fushan Shi
%A Houhui Song
%A Huanan Wang
%A Mohammed Kouadir
%A Yang Yang
%J Archive of "Cell Death & Disease".
%D 2019
%R 10.1038/s41419-019-1413-8
%X NLRP3 activator-induced K+ efflux leads to mitochondrial damage and mtROS production, which can induce enrichment of CLICs in plasma membrane to promote Cl¨C efflux. CLIC-mediated Cl¨C efflux can promote NEK7¨CNLRP3 interaction and subsequent NLRP3 inflammasome assembly. Excessive Ca2+ released from ER causes mitochondrial Ca2+ overload and mitochondrial damage, leading to mtROS production, which triggers NLRP3 inflammasome activation. The newly identified component of NLRP3 inflammasome NEK7, which can directly bind to NLRP3 protein, also requires K+ efflux, ROS production, and Cl¨C efflux for NLRP3 inflammasome assembl
%U https://www.ncbi.nlm.nih.gov/pmc/articles/PMC6372664/