Login / Signup

P2X7 Receptor in Alcoholic Steatohepatitis and Alcoholic Liver Fibrosis.

Guo-Qing XiaQian FangJun-Nan CaiZi-Xuan LiFeng-Zhi ZhangXiong-Wen Lv
Published in: Journal of clinical and translational hepatology (2022)
Alcoholic liver disease is one of the most common chronic liver diseases in the world. It is a liver disease caused by prolonged heavy drinking and its main clinical features are nausea, vomiting, enlargement of the liver, and jaundice. Recent studies suggest that Kupffer cell-mediated inflammatory response is a core driver in the development of alcoholic steatohepatitis and alcoholic liver fibrosis. As a danger signal, extracellular ATP activates the assembly of NLPR3 inflammasome by acting on purine P2X7 receptor, the activated NLRP3 inflammasome prompts ASC to cleave pro-cCaspase-1 into active caspase-1in KCs. Active caspase-1 promotes the conversion of pro-IL-1β to IL-1β, which further enhances the inflammatory response. Here, we briefly review the role of the P2X7R-NLRP3 inflammasome axis in the pathogenesis of alcoholic liver disease and the evolution of alcoholic steatohepatitis and alcoholic liver fibrosis. Regulation of the inflammasome axis of P2X7R-NLRP3 may be a new approach for the treatment of alcoholic liver disease.
Keyphrases
  • liver fibrosis
  • nlrp inflammasome
  • liver injury
  • drug induced
  • inflammatory response
  • cell death
  • immune response
  • cell therapy
  • mesenchymal stem cells
  • binding protein