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. 2023 Aug 28;16(9):1211. doi: 10.3390/ph16091211

Figure 1.

Figure 1

Proposed mechanism of NLRP3 inflammasome priming and activation in atherosclerosis. Recognition of DAMPs and PAMPs by toll-like receptors (TLRs) leads to the transcriptional activation of inflammasome components and the proinflammatory cytokines pro-interleukin(IL)-1 and pro-IL-18. During the activation phase, cholesterol crystals induce lysosomal destabilization and rupture, with the release of cathepsins. Those molecules promote NLRP3 inflammasome activation directly or indirectly through mitochondrial (MC) dysfunction and the release of mitochondrial DNA and reactive oxygen species (ROS). Following NLRP3 inflammasome formation, the autoproteolytic cleavage of caspase (CASP)-1 within the complex ensues and active CASP-1 ultimately cleaves pro-IL-1β and pro-IL-18 into their active forms, enhancing inflammation and atherosclerosis progression. CARD: caspase recruitment domain, PYD: pyrin domain.