NLRP3 Inflammasome and Inflammatory Diseases

Figure 1

NLRP3 inflammasome-mediated inflammation and autophagy have complex and bidirectional regulatory effects. After being stimulated by Ca²⁺, K⁺, or ROS, the NLRP3 inflammasome is activated and recruits and activates procaspase-1 to generate active caspase-1, which then converts the cytokine precursor pro-IL-1β or other proinflammatory cytokines into mature and biologically active forms and triggers a series of inflammatory responses and pyroptotic cell death. However, this process can be regulated and interrupted by autophagy via damage of NLRP3 inflammasome; however, NLRP3 can promote cell autophagy via activation of the G-protein RalB. Interestingly, the relationship between NLRP3 and autophagy is not definitively understood, and there have also been reports that contradict the above statement such as NF-κB activation can modulate the NLRP3 and autophagy in same direction.