Open AccessCrosstalk network among multiple inflammatory mediators in liver fibrosis
Author(s) -
Hanjing Zhangdi,
Si-Biao Su,
Fei Wang,
Ziyu Liang,
Yunqi Yan,
Shanyu Qin,
HaiXing Jiang
Publication year - 2019
Publication title -
world journal of gastroenterology
Language(s) - Uncategorized
Resource type - Journals
SCImago Journal Rank - 1.427
H-Index - 155
eISSN - 2219-2840
pISSN - 1007-9327
DOI - 10.3748/wjg.v25.i33.4835
Subject(s) - crosstalk , fibrosis , hepatic stellate cell , proinflammatory cytokine , inflammation , signal transduction , cirrhosis , pathogenesis , chronic liver disease , immunology , medicine , cytokine , liver disease , cancer research , biology , pathology , microbiology and biotechnology , physics , optics
Liver fibrosis is the common pathological basis of all chronic liver diseases, and is the necessary stage for the progression of chronic liver disease to cirrhosis. As one of pathogenic factors, inflammation plays a predominant role in liver fibrosis via communication and interaction between inflammatory cells, cytokines, and the related signaling pathways. Damaged hepatocytes induce an increase in pro-inflammatory factors, thereby inducing the development of inflammation. In addition, it has been reported that inflammatory response related signaling pathway is the main signal transduction pathway for the development of liver fibrosis. The crosstalk regulatory network leads to hepatic stellate cell activation and proinflammatory cytokine production, which in turn initiate the fibrotic response. Compared with the past, the research on the pathogenesis of liver fibrosis has been greatly developed. However, the liver fibrosis mechanism is complex and many pathways involved need to be further studied. This review mainly focuses on the crosstalk regulatory network among inflammatory cells, cytokines, and the related signaling pathways in the pathogenesis of chronic inflammatory liver diseases. Moreover, we also summarize the recent studies on the mechanisms underlying liver fibrosis and clinical efforts on the targeted therapies against the fibrotic response.