Topic Highlights Open Access
Copyright ©2009 The WJG Press and Baishideng. All rights reserved.
World J Gastroenterol. Mar 14, 2009; 15(10): 1162-1162
Published online Mar 14, 2009. doi: 10.3748/wjg.15.1162
Alcohol and liver
Natalia A Osna, Department of Internal Medicine, University of Nebraska Medical Center, Liver Study Unit R151, VA Medical Center, 4101 Woolworth Ave, Omaha, NE 68105, United States
Author contributions: This review was written by Osna NA.
Correspondence to: Natalia A Osna, MD, PhD, Department of Internal Medicine, University of Nebraska Medical Center, Liver Study Unit R151, VA Medical Center, 4101 Woolworth Ave, Omaha, NE 68105, United States. nosna@unmc.edu
Telephone: +1-402-9953735
Fax: +1-402-4490604
Received: December 25, 2008
Revised: January 15, 2009
Accepted: January 22, 2009
Published online: March 14, 2009

Abstract

FROM THE EDITOR

Liver is a primary site of ethanol metabolism, which makes this organ susceptible to alcohol-induced damage. Alcoholic liver disease (ALD) has many manifestations and complicated pathogenesis. In this Topic Highlight, we included the key reviews that characterize new findings about the mechanisms of ALD development and might be of strong interest for clinicians and researchers involved in liver alcohol studies.

Being the primary site of alcohol metabolism, liver is severely influenced by alcohol drinking. The combination of toxic effects of alcohol and numerous predisposing factors usually form the basis for ALD development. This disease has many manifestations, which are triggered by multiple pathogenic factors, causing progression in liver damage from steatosis to liver cirrhosis and hepatocarcinoma. The progression between various stages of ALD is driven by so-called “second hits”, which trigger ALD development. In 2007, in World Journal of Gastroenterology, we published Topic Highlight: Alcohol liver injury: Pathological feature and models. There, we reviewed the role of alcohol in changes of iron metabolism, proteasome function, immune response, signaling mechanisms, transmethylation reactions, as well as apoptosis and mitochondrial damage. Current Topic Highlight is a logical continuation of the previous one, which further expands our understanding of the mechanisms of ALD progression and complexity of ALD pathogenesis, thereby providing important information for hepatologists about the modern directions in alcohol research.

ADDITIONAL FILE

1 Bardag-Gorce F. Nuclear effects of ethanol-induced proteasome inhibition in liver cells. World J Gastroenterol 2009; 15: 1163-1167

2 Dolganiuc A, Szabo G. In vitro and in vivo models of acute alcohol exposure. World J Gastroenterol 2009; 15: 1168-1177

3 Donohue TM Jr. Autophagy and ethanol-induced liver injury. World J Gastroenterol 2009; 15: 1178-1185

4 Harrison-Findik DD. Is the iron regulatory hormone hepcidin a risk factor for alcoholic liver disease? World J Gastroenterol 2009; 15: 1186-1193

5 Lee SML, Casey CA, McVicker BL. Impact of asialoglycoprotein receptor deficiency on the development of liver injury. World J Gastroenterol 2009; 15: 1194-1200

6 Osna NA. Hepatitis C virus and ethanol alter antigen presentation in liver cells. World J Gastroenterol 2009; 15: 1201-1208

7 Schaffert CS, Duryee MJ, Hunter CD, Hamilton BC 3rd, DeVeney AL, Huerter MM, Klassen LW, Thiele GM. Alcohol metabolites and lipopolysaccharide: Roles in the development and/or progression of alcoholic liver disease. World J Gastroenterol 2009; 15: 1209-1218

8 Shepard BD, Tuma PL. Alcohol-induced protein hyperacetylation: Mechanisms and consequences. World J Gastroenterol 2009; 15: 1219-1230

Footnotes

S- Editor Li LF L- Editor Wang XL E- Editor Yin DH

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