NLRP3 Inflammasome: A Potential Alternative Therapy Target for Atherosclerosis

Figure 3

Activation of the NLRP3 inflammasome. Priming is initiated by the TLRs, which recognize and combine the corresponding signals to activate NF-κB at the transcriptional level, facilitating the expression of NLRP3 and various inflammatory precursors, such as IL-1β and IL-18 precursors in preparation for the next inflammatory response. NLRP3 is activated by related ligands via ionic flux (I), lysosome rupture and cathepsin B release (II), mitochondrial injury and reactive oxygen species (ROS) generation (III), and endoplasmic reticulum (ER) stress (IV). NLRP3 recruits ASC and procaspase-1 to assemble into the NLRP3 inflammasome. NLRP3 inflammasome which includes mature caspase-1 can promote the activation of proinflammatory mediators such as IL-1β and IL-18 and promote the occurrence of inflammatory response.