Progress in inflammasome activation and pyrolysis in alcoholic liver disease

Alcoholic liver disease (ALD) is a chronic liver disease characterized by large accumulation of lipids in the liver, accompanied by inflammation, fibrosis, cirrhosis, and hepatocellular carcinoma. In the different stages of ALD, mediators of the immune system, such as cytokines or inflammasomes, are crucially involved. In the ALD disease spectrum, the upregulation of the inflammatory cascade is the main factor in the development of steatohepatitis into severe alcoholic hepatitis. Activation of the inflammatory cascade requires multiple stimuli. Pyroptosis is a new type of programmed cell death that relies on caspase. Inflammasomes play a crucial role in the process of cell death. Cellular infection or cellular stress can activate inflammatory corpuscles, leading to assembly of inflammasome polyprotein complexes, activation of caspase-1 and its downstream substrates pro-IL-1β, pro-IL-18 and gasdermin D activation and maturation, thus participating in the body's immune inflammatory response and induced cell death. In recent years, there is increasing evidence that activation of inflammatory bodies and pyroptosis play a key role in the development of alcoholic liver disease.