FIGURE 2.

Multiple effects of radiation on NLRP3 inflammasome activation. Radiation-induced NF-κB activation is responsible for the upregulation of NLRP3 and pro-interleukin-1β. Second signals come from multiple pathways: water radiolysis, K⁺ efflux, endoplasmic reticulum (ER) stress, mitochondrial dysfunction, ceramide pathway, and lysosomal rupture pathways, most of which appear to converge in the production of reactive oxygen species (ROS). The primary and secondary signals triggers the NLRP3 inflammasome activation, resulting in the maturation of caspase 1 and IL-1β. Two evolutionarily conserved degradation pathways, ubiquitin-proteasome and autophagy, negatively regulate NLRP3 activation.