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. 2021 May 29;13:17590914211018100. doi: 10.1177/17590914211018100

Figure 2.

Figure 2.

Main Mechanism of NLRP3 Inflammasome in Development of Atherosclerosis. The phagocytosis of ox-LDL generates ROS through the cathepsin B pathway to activate the NLRP3 inflammasome. Activation of the NLRP3 inflammasome accelerates neutrophil and macrophage recruitment, increases the susceptibility of macrophages to lipid deposition, promotes foam cell formation, induces macrophages secreting IL-1β, and impairs plaque stability. Rupture of atherosclerotic plaques can cause stroke. Ox-LDL also upregulates the expression of the pro-IL-1β. IL-1β inhibits cholesterol efflux through a negative feedback, results in accumulation of intracellular cholesterol and foam cell formation. CD36 converts intracellular soluble ligands into crystals or fibrils, while UDCA increases cholesterol solubility, decreases cholesterol crystals-depositions, and inhibits NLRP3 inflammasome dependent inflammation. HDL play a protective role in atherosclerosis by suppressing monocyte cell recruitment and IL-1β secretion. Abbreviations: ox-LDL: oxidized low-density lipoprotein, ROS: reactive oxygen species, UDCA: ursodeoxycholic acid, HDL: high-density lipoproteins.