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Biological Chemistry

Editor-in-Chief: Brüne, Bernhard

Editorial Board Member: Buchner, Johannes / Ludwig, Stephan / Sies, Helmut / Turk, Boris / Wittinghofer, Alfred

12 Issues per year



Mechanisms and cell signaling in alcoholic liver disease

Juliane I. Beier1, 2 / Craig J. McClain1–4, , ,

1Department of Pharmacology and Toxicology, University of Louisville Health Sciences Center, Louisville, KY 40292, USA

2University of Louisville Alcohol Research Center, Louisville, KY 40292, USA

3Department of Medicine, University of Louisville, Louisville, KY 40292, USA

4Louisville VA Medical Center, Louisville, KY 40292, USA

Corresponding author

Citation Information: Biological Chemistry. Volume 391, Issue 11, Pages 1249–1264, ISSN (Online) 1437-4315, ISSN (Print) 1431-6730, DOI: 10.1515/bc.2010.137, September 2010

Publication History

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Alcoholic liver disease (ALD) remains a major cause of morbidity and mortality worldwide. For example, the Veterans Administration Cooperative Studies reported that patients with cirrhosis and superimposed alcoholic hepatitis had a 4-year mortality of >60%. The poor prognosis of ALD implies that preventing disease progression would be more effective than treating end-stage liver disease. An obvious avenue of prevention would be to remove the damaging agent; however, the infamously high rate of recidivism in alcoholics makes maintaining abstinence a difficult treatment goal to prevent ALD. Indeed, although the progression of ALD is well-characterized, there is no universally accepted therapy available to halt or reverse this process in humans. With better understanding of the mechanism(s) and risk factors that mediate the initiation and progression of ALD, rational targeted therapy can be developed to treat or prevent ALD. The purpose of this review is to summarize the established and proposed mechanisms by which chronic alcohol abuse damages the liver and to highlight key signaling events known or hypothesized to mediate these effects.

Keywords: alcohol metabolism; alcoholic liver disease; cytokines; inflammation; oxidative stress

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