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

NLRP3 activator-induced K+ efflux leads to mitochondrial damage and mtROS production, which can induce enrichment of CLICs in plasma membrane to promote Cl– efflux. CLIC-mediated Cl– efflux can promote NEK7–NLRP3 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– efflux for NLRP3 inflammasome assembl