Figure 4.

The mechanisms of the effects of autophagy on NLRP3 inflammasome. NLRP3-activating signals, such as cholesterol crystals, cause damage to lysosomes and mitochondria, resulting in cathepsin release, ROS release, and K+ excretion. It leads to the assembly and activation of inflammasomes, followed by the formation of active caspase-1. Inflammation is aided by active caspase-1, which converts pro-forms of IL-1β and IL-18 into their mature forms. Mitophagy and autophagy are both able to decrease mtROS production by clearing the damaged mitochondria, thus inhibiting NLRP3 inflammasomes. In addition, the NLRP3 protein was discovered to be a substrate for chaperone-mediated autophagy and was degraded into the lysosome by this pathway. The arrows represent the promotion, and the blunt arrows represent the inhibition.