Mechanisms and cell signaling in alcoholic liver disease
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Juliane I. Beier
Abstract
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.
©2010 by Walter de Gruyter Berlin New York
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Articles in the same Issue
- Guest Editorial
- Highlight: Xenobiotics and Cell Signaling
- Reviews
- An introduction to the molecular basics of aryl hydrocarbon receptor biology
- Mechanisms and cell signaling in alcoholic liver disease
- Superoxide anion and hydrogen peroxide-induced signaling and damage in angiotensin II and aldosterone action
- Breakdown products of neoglucobrassicin inhibit activation of Nrf2 target genes mediated by myrosinase-derived glucoraphanin hydrolysis products
- Cadmium ions promote monocytic differentiation of human leukemia HL-60 cells treated with 1α,25-dihydroxyvitamin D3
- Zonation of heme synthesis enzymes in mouse liver and their regulation by β-catenin and Ha-ras
- The C2-streptavidin delivery system promotes the uptake of biotinylated molecules in macrophages and T-leukemia cells
- Short Communications
- c-Src-mediated activation of Erk1/2 is a reaction of epithelial cells to carbon nanoparticle treatment and may be a target for a molecular preventive strategy
- Loss of gap junctional intercellular communication in rat lung epithelial cells exposed to carbon or silica-based nanoparticles
- Review
- Lipoprotein receptors – an evolutionarily ancient multifunctional receptor family
