【摘要】 细胞焦亡是依赖于caspase-1和/或caspase-11,并伴有大量炎性因子释放的新型细胞程序性死亡。外界刺激通过信号通路作用于不同炎症小体,进而激活caspase-1和/或caspase-11,介导细胞渗透性肿胀破裂,形成细胞膜小孔,释放大量炎性因子,诱导细胞死亡。在肝纤维化、病毒性肝炎等多种肝脏疾病中细胞焦亡增强,而肝癌组织中细胞焦亡被抑制。本文就细胞焦亡的机制以及在肝硬化、病毒性肝炎、酒精性肝病、非酒精性脂肪性肝病、肝细胞癌发生、发展中作用的研究进展作一综述。更多还原

【Abstract】 Pyroptosis is a novel programmed cell death depending on caspase-1/caspase-11 and is accompanied by the release of a large number of inflammatory cytokines. External stimuli act on differential inflammatory cells through signaling pathways, which activates caspase-1/caspase-11, intermediates osmotic swell and disruption of cells, forms small pores in the cell membrane, and induces cell death by releasing a large number of inflammatory factors. Pyroptosis is enhanced in liver fibrosis, viral hepatitis and other liver diseases, while it is inhibited in liver cancer tissue. This paper reviews the research progress of the mechanism of pyroptosis as well as its role in the development of liver diseases as cirrhosis, viral hepatitis, alcoholic liver disease, non-alcoholic fatty liver disease and hepatocellular carcinoma.更多还原