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• W4310367340 startingPage "159" @default.
• W4310367340 abstract "The inflammasomes are cytosolic multiprotein complexes that induce inflammation and pyroptotic cell death in response to both pathogens and endogenous activators. Assembly of the inflammasome leads to caspase-1-dependent release of the proinflammatory cytokines, IL-1β and IL-18, as well as to gasdermin D-mediated pyroptotic cell death. Autophagy, an intracellular homeostatic mechanism, is responsible for delivering cytosolic macromolecules and organelles, as well as pathogens to lysosomes for degradation and amino acid recycling. The autophagy dysfunction results in hyperinflammation and excessive activation of inflammasomes. Autophagic removal of inflammasome activators, like mitochondrial ROS, inflammasome components, and cytokines, can reduce inflammation. Inflammasome signaling pathways can regulate autophagy for balance between inflammatory response and prevention of excessive inflammation. In this chapter, we discuss recent advances in the involvement of autophagy in regulating NLRP3 and AIM2 inflammasomes activation and their implication in sepsis." @default.
• W4310367340 created "2022-12-09" @default.
• W4310367340 creator A5056184136 @default.
• W4310367340 creator A5081855803 @default.
• W4310367340 date "2023-01-01" @default.
• W4310367340 modified "2023-09-25" @default.
• W4310367340 title "Autophagy and the inflammasome" @default.
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