Review
Copyright ©2006 Baishideng Publishing Group Co., Limited. All rights reserved.
World J Gastroenterol. Nov 21, 2006; 12(43): 6926-6932
Published online Nov 21, 2006. doi: 10.3748/wjg.v12.i43.6926
Role of ethanol in the regulation of hepatic stellate cell Function
Jian-Hua Wang, Robert G Batey, Jacob George
Jian-Hua Wang, Jacob George, Storr Liver Unit, Westmead Millennium Institute, University of Sydney and Westmead Hospital, Westmead, New South Wales, Australia
Robert G Batey, Drug and Alcohol Clinical Services, Hunter New England Area Health Service, Locked Bag 119, Wallsend, New South Wales 2287, Australia
Author contributions: All authors contributed equally to the work.
Correspondence to: Jian-Hua Wang, PhD, MD, Senior Research Officer, Storr Liver Unit, Westmead Millennium Institute, University of Sydney, Westmead 2145, Australia. jianhua_wang@wmi.usyd.edu.au
Telephone: +61-2-98459132 Fax: +61-2-98459103
Received: July 18, 2006
Revised: September 12, 2006
Accepted: September 19, 2006
Published online: November 21, 2006
Abstract

Evidence has accumulated to suggest an important role of ethanol and/or its metabolites in the pathogenesis of alcohol-related liver disease. In this review, the fibrogenic effects of ethanol and its metabolites on hepatic stellate cells (HSCs) are discussed. In brief, ethanol interferes with retinoid metabolism and its signaling, induces the release of fibrogenic cytokines such as transforming growth factor β-1 (TGFβ-1) from HSCs, up-regulates the gene expression of collagen I and enhances type I collagen protein production by HSCs. Ethanol further perpetuates an activated HSC phenotype through extracellular matrix remodeling. The underlying pathophysiologic mechanisms by which ethanol exerts these pro-fibrogenic effects on HSCs are reviewed.

Keywords: Ethanol, Acetaldehyde, Hepatic stellate cells, liver fibrosis, Type I collagen gene, Transcription factors, Transforming growth factor β-1