Evidence map›Paper›PMID 22829816›Full record

ArticleJournal of toxicology2012

Oxidative Stress and the ER Stress Response in a Murine Model for Early-Stage Alcoholic Liver Disease.

James J Galligan, Rebecca L Smathers, Colin T Shearn, Kristofer S Fritz, Donald S Backos, Hua Jiang, Christopher C Franklin, David J Orlicky, Kenneth N Maclean, Dennis R Petersen

Open access · goldAbstract read
In one paragraph

Article in Journal of toxicology, 2012. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 59 papers, 2 of them syntheses that pooled it.

0numbers the graph read from it
0cells of the map it votes in
59citing papers in PubMed, 2 pooled it
4.8field-weighted citation impact, top 5% of its field
1 · What the graph read from it

What it found

Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.

The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.

2 · The registry

The trial behind it

Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.

Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.

3 · Its place in the literature

Who cites it

59 citing papers in PubMed, 2 syntheses or guidelines pooled it, 100 citations in OpenAlex.

  1. Pooled it
  2. HFE genetic variability and risk of alcoholic liver disease: A meta-analysis.Journal of Huazhong University of Science and Technology. Medical sciences = Hua zhong ke ji da xue xue bao. Yi xue Ying De wen ban = Huazhong keji daxue xuebao. Yixue Yingdewen ban · 2016
    Pooled it
  3. Trial
  4. Review
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  7. Article
  8. Aging · 2023
    Article
  9. Dietary cholesterol in alcohol-associated liver disease.Immunometabolism (Cobham, Surrey) · 2023
    Review
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  11. Article
  12. Article
  13. Review
  14. Article
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4 · The record

Corrections and comments

PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.

5 · Who and what money

Authors and funding

10 authors at 1 institution in 1 country.

James J GalliganDepartment of Pharmacology, University of Colorado Anschutz Medical Campus, Aurora, CO 80045, USA.
Rebecca L Smathers
Colin T Shearn
Kristofer S Fritz
Donald S Backos
Hua Jiang
Christopher C Franklin
David J Orlicky
Kenneth N Maclean
Dennis R Petersen
University of Colorado Anschutz Medical Campus · US

Funding

Lipid Aldehyde and Ethanol Induced Liver DamageR37AA009300 · NIAAA · UNIVERSITY OF COLORADO DENVER · PI PETERSEN, DENNIS · 2008 to 2017
$4.4M
Proteomic profiling of NASH: disease mechanisms and novel treatmentR01DK074487 · NIDDK · UNIVERSITY OF COLORADO DENVER · PI PETERSEN, DENNIS · 2007 to 2011
$1.5M
Modification of PDI by 4-HNE and 4-ONE and its Role in Ethanol-Induced ER StressF31AA018606 · NIAAA · UNIVERSITY OF COLORADO DENVER · PI GALLIGAN, JAMES J · 2009 to 2011
$77k
NIAAA NIH HHS F31 AA018606NIAAA NIH HHS R37 AA009300NIDDK NIH HHS R01 DK074487
6 · The paper itself

Abstract

Alcoholic liver disease (ALD) is a primary cause of morbidity and mortality in the United States and constitutes a significant socioeconomic burden. Previous work has implicated oxidative stress and endoplasmic reticulum (ER) stress in the etiology of ALD; however, the complex and interrelated nature of these cellular responses presently confounds our understanding of ethanol-induced hepatopathy. In this paper, we assessed the pathological contribution of oxidative stress and ER stress in a time-course mouse model of early-stage ALD. Ethanol-treated mice exhibited significant hepatic panlobular steatosis and elevated plasma ALT values compared to isocaloric controls. Oxidative stress was observed in the ethanol-treated animals through a significant increase in hepatic TBARS and immunohistochemical staining of 4-HNE-modified proteins. Hepatic glutathione (GSH) levels were significantly decreased as a consequence of decreased CBS activity, increased GSH utilization, and increased protein glutathionylation. At the same time, immunoblot analysis of the PERK, IRE1α, ATF6, and SREBP pathways reveals no significant role for these UPR pathways in the etiology of hepatic steatosis associated with early-stage ALD. Collectively, our results indicate a primary pathogenic role for oxidative stress in the early initiating stages of ALD that precedes the involvement of the ER stress response.

Identifiers

PMID22829816
PMCPMC3399426
OpenAlexW1999780173

What OpenQuestion holds

Textmetadata
LicenceCC BY
Read underepoch 390

Registered trials

None linked

Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.