Journal of Gastroenterology

, Volume 43, Issue 6, pp 419–428

Molecular mechanism of hepatic stellate cell activation and antifibrotic therapeutic strategies

  • Jing-Ting Li
  • Zhang-Xiu Liao
  • Jie Ping
  • Dan Xu
  • Hui Wang
Review

DOI: 10.1007/s00535-008-2180-y

Cite this article as:
Li, JT., Liao, ZX., Ping, J. et al. J Gastroenterol (2008) 43: 419. doi:10.1007/s00535-008-2180-y

Abstract

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.

Key words

hepatic stellate cells activation liver fibrosis molecular mechanism 

Copyright information

© Springer Japan 2008

Authors and Affiliations

  • Jing-Ting Li
    • 1
  • Zhang-Xiu Liao
    • 1
  • Jie Ping
    • 1
  • Dan Xu
    • 1
  • Hui Wang
    • 1
  1. 1.Department of PharmacologyBasic Medical School of Wuhan UniversityWuhanChina

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