SMAD公司
信号转导
肝星状细胞
细胞外基质
肝纤维化
纤维化
转化生长因子
细胞生物学
斯达
转化生长因子β
生物
癌症研究
免疫学
医学
病理
内分泌学
车站3
作者
Jing Li,Wei Wang,Jilong Shen
摘要
Liver fibrosis is characterized by an abnormal hepatic accumulation of extracellular matrix (ECM) that results from both increased deposition and reduced degradation of collagen fibres. Some studies show that transforming growth factor beta1 (TGF-beta1), alternatively activated macrophage (aaM) and interleukin 13 (IL-13) play a key role in the evolution of fibrosis, of which TGF-beta1 and IL-13 become research hotspots. TGF-beta1 mainly activates hepatic stellate cells (HSC) through TGF-beta1/Smad signal pathway, while IL-13 seems to play a rather crucial role through JAK-STAT6 signal pathway. aaM is an important source of TGF-beta1 and activated with IL-13. This paper reviews the role of those signaling molecules in cellular signal transduction of hepatic fibrosis of schistosomiasis japonica, and provides some targets for future drug development.
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