焦亡在酒精性肝病发病机制中的作用

Effect of pyroptosis in the pathogenesis of alcoholic liver disease

长期摄入大量乙醇导致肠源性内毒素血症,活性氧、高浓度的三磷酸腺苷及尿酸激活焦亡系统,进而通过切割Gasdermin-D打孔机制导致肝细胞死亡,同时伴有白细胞介素-1β、白细胞介素-18等炎性因子的释放。这一系列的过程激活免疫系统,介导级联炎症反应,促进酒精性肝病从脂肪变性到炎症、纤维化的进展。

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.