Document Detail


Autophagy in alcohol-induced liver diseases.
MedLine Citation:
PMID:  22551004     Owner:  NLM     Status:  MEDLINE    
Abstract/OtherAbstract:
Alcohol is the most abused substance worldwide and a significant source of liver injury; the mechanisms of alcohol-induced liver disease are not fully understood. Significant cellular toxicity and impairment of protein synthesis and degradation occur in alcohol-exposed liver cells, along with changes in energy balance and modified responses to pathogens. Autophagy is the process of cellular catabolism through the lysosomal-dependent machinery, which maintains a balance among protein synthesis, degradation, and recycling of self. Autophagy is part of normal homeostasis and it can be triggered by multiple factors that threaten cell integrity, including starvation, toxins, or pathogens. Multiple factors regulate autophagy; survival and preservation of cellular integrity at the expense of inadequately folded proteins and damaged high-energy generating intracellular organelles are prominent targets of autophagy in pathological conditions. Coincidentally, inadequately folded proteins accumulate and high-energy generating intracellular organelles, such as mitochondria, are damaged by alcohol abuse; these alcohol-induced pathological findings prompted investigation of the role of autophagy in the pathogenesis of alcohol-induced liver damage. Our review summarizes the current knowledge about the role and implications of autophagy in alcohol-induced liver disease.
Authors:
Angela Dolganiuc; Paul G Thomes; Wen-Xing Ding; John J Lemasters; Terrence M Donohue
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Publication Detail:
Type:  Journal Article; Research Support, N.I.H., Extramural; Research Support, Non-U.S. Gov't; Review     Date:  2012-05-02
Journal Detail:
Title:  Alcoholism, clinical and experimental research     Volume:  36     ISSN:  1530-0277     ISO Abbreviation:  Alcohol. Clin. Exp. Res.     Publication Date:  2012 Aug 
Date Detail:
Created Date:  2012-08-06     Completed Date:  2012-12-11     Revised Date:  2013-08-14    
Medline Journal Info:
Nlm Unique ID:  7707242     Medline TA:  Alcohol Clin Exp Res     Country:  England    
Other Details:
Languages:  eng     Pagination:  1301-8     Citation Subset:  IM    
Copyright Information:
Copyright © 2012 by the Research Society on Alcoholism.
Affiliation:
Department of Internal Medicine, University of Florida, Gainesville, USA. angela.dolganiuc@medicine.ufl.edu
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MeSH Terms
Descriptor/Qualifier:
Animals
Autophagy / physiology*
Biological Markers
Cell Death / drug effects
Central Nervous System Depressants / toxicity
Disease Models, Animal
Ethanol / toxicity
Humans
Liver Diseases, Alcoholic / pathology*
Mitochondria, Liver / drug effects,  metabolism,  pathology
Phagosomes / metabolism
Proteins / metabolism
Signal Transduction / drug effects
TOR Serine-Threonine Kinases / metabolism
Toll-Like Receptors / drug effects
Grant Support
ID/Acronym/Agency:
C06RR015455/RR/NCRR NIH HHS; P01DK59340/DK/NIDDK NIH HHS; P20 GM103418/GM/NIGMS NIH HHS; P20RR016475/RR/NCRR NIH HHS; P20RR021940/RR/NCRR NIH HHS; R01 AA020518/AA/NIAAA NIH HHS; R01AA017212/AA/NIAAA NIH HHS; R01AA02518/AA/NIAAA NIH HHS; R01CA119079/CA/NCI NIH HHS; R01DK073336/DK/NIDDK NIH HHS; R01DK37034/DK/NIDDK NIH HHS; R21 AA017421/AA/NIAAA NIH HHS; R21AA016571/AA/NIAAA NIH HHS; R21AA017421/AA/NIAAA NIH HHS
Chemical
Reg. No./Substance:
0/Biological Markers; 0/Central Nervous System Depressants; 0/Proteins; 0/Toll-Like Receptors; 64-17-5/Ethanol; EC 2.7.1.1/TOR Serine-Threonine Kinases
Comments/Corrections

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