Document Detail


The contribution of endoplasmic reticulum stress to liver diseases.
MedLine Citation:
PMID:  21384408     Owner:  NLM     Status:  MEDLINE    
Abstract/OtherAbstract:
The unfolded protein response (UPR) is an evolutionarily conserved cell signaling pathway that is activated to regulate protein synthesis and restore homeostatic equilibrium when the cell is stressed from increased client protein load or the accumulation of unfolded or malfolded proteins. Once activated, this signaling pathway can either result in the recovery of homeostasis or can activate a cascade of events that ultimately result in cell death. The UPR/endoplasmic reticulum (ER) stress response spectrum and its interplay with other cellular organelles play an important role in the pathogenesis of disease in secretory cells rich in ER, such as hepatocytes. Over the past 2 decades, the contribution of ER stress to various forms of liver diseases has been examined. Robust support for a contributing, as opposed to a secondary role, for ER stress response is seen in the nonalcoholic steatohepatitis, alcoholic liver disease, ischemia/reperfusion injury, and cholestatic models of liver disease. The exact direction of the cause and effect relationship between modes of cell injury and ER stress remains elusive. It is apparent that a complex interplay exists between ER stress response, conditions that promote it, and those that result from it. A vicious cycle in which ER stress promotes inflammation, cell injury, and steatosis and in which steatogenesis, inflammation, and cell injury aggravate ER stress seems to be at play. It is perhaps the nature of such a vicious cycle that is the key pathophysiologic concept. Therapeutic approaches aimed at interrupting the cycle may dampen the stress response and the ensuing injury.
Authors:
Lily Dara; Cheng Ji; Neil Kaplowitz
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Publication Detail:
Type:  Journal Article; Research Support, N.I.H., Extramural    
Journal Detail:
Title:  Hepatology (Baltimore, Md.)     Volume:  53     ISSN:  1527-3350     ISO Abbreviation:  Hepatology     Publication Date:  2011 May 
Date Detail:
Created Date:  2011-04-26     Completed Date:  2011-07-19     Revised Date:  2012-05-02    
Medline Journal Info:
Nlm Unique ID:  8302946     Medline TA:  Hepatology     Country:  United States    
Other Details:
Languages:  eng     Pagination:  1752-63     Citation Subset:  IM    
Copyright Information:
Copyright © 2011 American Association for the Study of Liver Diseases.
Affiliation:
University of Southern California Research Center for Liver Diseases, Los Angeles, CA, USA. lily.dara@usc.edu
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MeSH Terms
Descriptor/Qualifier:
Animals
Drug-Induced Liver Injury / etiology
Endoplasmic Reticulum / physiology*
Fatty Liver / etiology
Hepatitis, Viral, Human / etiology
Humans
Hyperhomocysteinemia / etiology
Liver Diseases / etiology*
Liver Diseases, Alcoholic / etiology
Stress, Physiological*
Unfolded Protein Response*
Grant Support
ID/Acronym/Agency:
P30 DK048522-16/DK/NIDDK NIH HHS; P30 DK48522/DK/NIDDK NIH HHS; P50 AA011999-12/AA/NIAAA NIH HHS; P50 AA11999/AA/NIAAA NIH HHS; R01 AA014428/AA/NIAAA NIH HHS; R01 AA014428-06A1/AA/NIAAA NIH HHS; R01 AA014428-07/AA/NIAAA NIH HHS; R01 AA018612/AA/NIAAA NIH HHS; R01 AA018612-01A1/AA/NIAAA NIH HHS; R01 AA018612-02/AA/NIAAA NIH HHS; R01 AA018846/AA/NIAAA NIH HHS; R01 AA018846-01/AA/NIAAA NIH HHS; R01 AA018846-02/AA/NIAAA NIH HHS; R01 AA018846-03/AA/NIAAA NIH HHS; R01 DK067215-05/DK/NIDDK NIH HHS; R01DK067215/DK/NIDDK NIH HHS

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