FIGURE 1.

Mechanisms of NLRP3 inflammasome activation. NLRP3 inflammasome must be primed, followed by activation. The priming step is activated by pathogen-associated molecular patterns (PAMPs) or cytokines, leading to transcriptional upregulation of NLRP3, pro-IL-1β, and pro-IL-18. The activation step is induced by numerous PAMPs or damage-associated molecular patterns (DAMPs), such as particulates, pore-forming toxins, and ATP. RNA viruses activate NLRP3 through mitochondrial antiviral signaling protein (MAVS) on the mitochondrial outer membrane. NLRP3 inflammasome activates caspase-1, which in turn cleaves pro-IL-1β and pro-IL-18. Gasdermin D (GSDMD) is also cleaved and inserted into the membrane, forming pores and inducing pyroptosis. GSDMDNterm, GSDMD amino-terminal cell death domain; NEK7, NIMA-related kinase 7; NF-κB, nuclear factor-κB; P2X₇, P2X purinoceptor 7; ROS, reactive oxygen species; TLR, Toll-like receptor; TNF, tumor necrosis factor; TNFR, tumor necrosis factor receptor; TWIK2, two-pore domain weak inwardly rectifying K+ channel 2. This figure was created with BioRender.com.