Fig. 1

Mechanisms of NLRP3 inflammasome activation. Decreases in intracellular K⁺ concentrations, increases in intracellular Ca²⁺ concentrations, and excessive ROS production activate the NLRP3 inflammasome. As an inhibitor of the TRX system, TXNIP has been proven to mediate generation of large amounts of ROS and to activate the NLRP3 inflammasome. The activation of P2X7R caused by elevated ATP concentrations leads to increased intracellular Ca²⁺ concentrations and K⁺ outflow, resulting in activation of the NLRP3 inflammasome. Cathepsin is released into the cytoplasm after lysosomal membrane rupture, which induces activation of the NLRP3 inflammasome via cleavage of NLRP3 receptor-associated inhibitory domains or inhibitory proteins. dsRNA, increased intracellular Ca²⁺ levels, K⁺ outflow, increased ROS and other cellular stress factors activate PKR, and PKR activates the NLRP3 inflammasome. Anaerobic glycolysis results in the accumulation of large amounts of H⁺ and lactic acid, causing acidosis and ultimately activating the NLRP3 inflammasome