Molecular mechanism of hepatic stellate cell activation and antifibrotic therapeutic strategies

Activation of hepatic stellate cells (HSCs) is the dominant event in liver fibrosis. The early events in the organization of HSC activation have been termed initiation. Initiation encompasses rapid changes in gene expression and phenotype that render the cells responsive to cytokines and other local...

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Bibliographic Details
Published in:Journal of gastroenterology 2008-06, Vol.43 (6), p.419-428
Main Authors: Li, Jing-Ting, Liao, Zhang-Xiu, Ping, Jie, Xu, Dan, Wang, Hui
Format: Article
Language:English
Subjects:
Abdominal Surgery
Animals
Apoptosis
Cell Proliferation
Chemotaxis
Colorectal Surgery
Cytokines - physiology
Gastroenterology
Hepatocytes - metabolism
Hepatocytes - physiology
Hepatology
Humans
Liver Cirrhosis - physiopathology
Liver Cirrhosis - therapy
Medicine
Medicine & Public Health
Review
Surgical Oncology
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Summary:Activation of hepatic stellate cells (HSCs) is the dominant event in liver fibrosis. The early events in the organization of HSC activation have been termed initiation. Initiation encompasses rapid changes in gene expression and phenotype that render the cells responsive to cytokines and other local stimuli. Cellular responses following initiation are termed perpetuation, which encompasses those cellular events that amplify the activated phenotype through enhanced growth factor expression and responsiveness. Multiple cells and cytokines play a part in the regulation of HSC activation. HSC activation consists of discrete phenotype responses, mainly proliferation, contractility, fibrogenesis, matrix degradation, chemotaxis and retinoid loss. Currently, antifibrotic therapeutic strategies include inhibition of HSC proliferation or stimulation of HSC apoptosis, downregulation of collagen production or promotion of its degradation, administration of cytokines, and infusion of mesenchymal stem cells. In this review, we summarize the latest advances in our understanding of the mechanisms of HSC activation and possible antifibrotic therapeutic strategies.
ISSN:0944-1174
1435-5922
DOI:10.1007/s00535-008-2180-y