细胞焦亡在肝纤维化发生、发展中的作用研究进展

细胞焦亡是一种新型的促炎程序性细胞死亡，不同于其他程序性死亡，包括经典途径和非经典途径，依赖于Caspase-1、Caspase-4、Caspase-5、Caspase-11介导。目前研究最为深入的是NLRP3炎症小体介导的依赖于Caspase-1的经典细胞焦亡途径，在机体免疫功能方面起到重要作用。研究表明细胞发生焦亡后可释放大量的促炎症细胞因子，这个细胞因子将进一步促进炎症的发展。近年来研究表明细胞焦亡在肝脏疾病的发生、发展中起重要作用。该文主要对细胞焦亡的分子机制及肝细胞、肝星状细胞和肝脏巨噬细胞与肝纤维化的关系进行综述。

Research advance in the role of pyroptosis in the development and progression of liver fibrosis

Pyroptosis is a new type of pro-inflammatory programmed cell death. Two different major categories of pathways, namely the Caspase-1-dependent classical pathway and the Caspase-4/5/11-dependent non-classical pathway, are involved in pyroptosis. Caspase-1-independent classical pathway mediated via NLRP3 inflammasome has been intensively studied and found to play an important role in immune function. Studies have shown that various pro-inflammatory cytokines can be released after pyroptosis, which will further aggravate the inflammation. In addition, pyroptosis is also critical for the development and progression of hepatic diseases. In this paper, we reviewed the molecular mechanism of pyroptosis and the relationship between the pyroptosis of hepatocytes, hepatic stellate cells, and hepatic macrophages, and liver fibrosis.