Intercellular crosstalk of hepatic stellate cells in liver fibrosis: New insights into therapy

被引:135
作者
Cai, Xuanyan [1 ]
Wang, Jiajia [1 ]
Wang, Jincheng [1 ]
Zhou, Qian [3 ]
Yang, Bo [1 ]
He, Qiaojun [1 ,2 ]
Weng, Qinjie [1 ,2 ]
机构
[1] Zhejiang Univ, Coll Pharmaceut Sci, Zhejiang Prov Key Lab Anticanc Drug Res, Hangzhou 310058, Peoples R China
[2] Zhejiang Univ, Ctr Drug Safety Evaluat & Res, Hangzhou 310058, Peoples R China
[3] Hangzhou Med Coll, Dept Pharm, Hangzhou 310053, Peoples R China
关键词
Liver fibrosis; Hepatic stellate cells; Intercellular crosstalk; Antifibrotic therapy; SINUSOIDAL ENDOTHELIAL-CELLS; KILLER T-CELLS; GROWTH-FACTOR; KUPFFER CELLS; FATTY LIVER; KAPPA-B; MOLECULAR-MECHANISMS; CELLULAR SENESCENCE; PARTIAL-HEPATECTOMY; PORTAL PRESSURE;
D O I
10.1016/j.phrs.2020.104720
中图分类号
R9 [药学];
学科分类号
100702 [药剂学];
摘要
Liver fibrosis is a dynamic wound-healing process characterized by the net accumulation of extracellular matrix. There is no efficient antifibrotic therapy other than liver transplantation to date. Activated hepatic stellate cells (HSCs) are the major cellular source of matrix-producing myofibroblasts, playing a central role in the initiation and progression of liver fibrosis. Paracrine signals from resident and inflammatory cells such as hepatocytes, liver sinusoidal endothelial cells, hepatic macrophages, natural killer/natural killer T cells, biliary epithelial cells, hepatic progenitor cells, and platelets can directly or indirectly regulate HSC differentiation and activation. Intercellular crosstalk between HSCs and those "responded" cells has been a critical event involved in HSC activation and fibrogenesis. This review summarizes recent advancement regarding intercellular communication between HSCs and other "responded cells" during liver fibrosis and experimental models of intercellular crosstalk systems, and provides novel ideas for potential antifibrotic therapeutic strategy.
引用
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页数:10
相关论文
共 168 条
[1]
Hepatic stellate cells regulate hepatic progenitor cells differentiation via the TGF-β1/Jagged1 signaling axis [J].
Aimaiti, Yasen ;
Jin, Xin ;
Shao, Yue ;
Wang, Wei ;
Li, Dewei .
JOURNAL OF CELLULAR PHYSIOLOGY, 2019, 234 (06) :9283-9296
[2]
Expression of cytochromes P450, conjugating enzymes and nuclear receptors in human hepatoma HepaRG cells [J].
Aninat, C ;
Piton, A ;
Glaise, D ;
Le Charpentier, T ;
Langouët, S ;
Morel, F ;
Guguen-Guillouzo, C ;
Guillouzo, A .
DRUG METABOLISM AND DISPOSITION, 2006, 34 (01) :75-83
[3]
Mouse models in non-alcoholic fatty liver disease and steatohepatitis research [J].
Anstee, QM ;
Goldin, RD .
INTERNATIONAL JOURNAL OF EXPERIMENTAL PATHOLOGY, 2006, 87 (01) :1-16
[4]
Aoyama T., 2010, HEPATOLOGY, V52, p447a
[5]
Barcena C., 2019, EBIOMEDICINE
[6]
Hepatitis B Virus Infection and Immunopathogenesis in a Humanized Mouse Model: Induction of Human-Specific Liver Fibrosis and M2-Like Macrophages [J].
Bility, Moses T. ;
Cheng, Liang ;
Zhang, Zheng ;
Luan, Yan ;
Li, Feng ;
Chi, Liqun ;
Zhang, Liguo ;
Tu, Zhengkun ;
Gao, Yanhang ;
Fu, Yangxin ;
Niu, Junqi ;
Wang, Fusheng ;
Su, Lishan .
PLOS PATHOGENS, 2014, 10 (03)
[7]
Generation of a humanized mouse model with both human immune system and liver cells to model hepatitis C virus infection and liver immunopathogenesis [J].
Bility, Moses T. ;
Zhang, Liguo ;
Washburn, Michael L. ;
Curtis, T. Anthony ;
Kovalev, Grigoriy I. ;
Su, Lishan .
NATURE PROTOCOLS, 2012, 7 (09) :1608-1617
[8]
BOROJEVIC R, 1985, IN VITRO CELL DEV B, V21, P382, DOI 10.1007/BF02623469
[9]
Pathophysiology of liver fibrosis and the methodological barriers to the development of anti-fibrogenic agents [J].
Bottcher, Katrin ;
Pinzani, Massimo .
ADVANCED DRUG DELIVERY REVIEWS, 2017, 121 :3-8
[10]
Regression of Liver Fibrosis [J].
Campana, Lara ;
Iredale, John P. .
SEMINARS IN LIVER DISEASE, 2017, 37 (01) :1-10