Abstract

Long-term intake of large amounts of ethanol leads to enterogenous endotoxemia. Reactive oxygen species, high concentrations of adenosine triphosphate and uric acid activate the pyroptosis system, which then cleaves the pore formation mechanism of gasdermin-D, leading to the death of liver cells, accompanied by the release of interleukin-1β, interleukin-18, and other inflammatory factors. This series of processes activates the immune system, mediates a cascade of inflammation, and promotes the development of alcoholic liver disease from steatosis to inflammation and fibrosis.

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