Evidence map›Paper›PMID 22960051›Full record

ReviewAlcohol (Fayetteville, N.Y.)2012

Rodent models of alcoholic liver disease: of mice and men.

Elizabeth Brandon-Warner, Laura W Schrum, C Max Schmidt, Iain H McKillop

Abstract readReview
In one paragraph

Review in Alcohol (Fayetteville, N.Y.), 2012. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 88 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
88citing papers in PubMed, 1 pooled it
6.5field-weighted citation impact, top 3% 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

88 citing papers in PubMed, 1 synthesis or guideline pooled it, 139 citations in OpenAlex.

  1. Pooled it
  2. c-Jun N-Terminal Kinase-2 Mediates Alcohol and Corticosterone-Induced Tissue Injury at the Gut-Liver Axis.FASEB journal : official publication of the Federation of American Societies for Experimental Biology · 2026
    Article
  3. Article
  4. Hepatic stellate cells in alcoholic liver cirrhosis: mechanisms of fibrogenesis, plasticity, and fibrosis reversal.Daru : journal of Faculty of Pharmacy, Tehran University of Medical Sciences · 2026
    Review
  5. Article
  6. Article
  7. Review
  8. Article
  9. Comparison of liver bile acid profiles in chronic alcohol feeding and NIAAA binge-on-chronic alcohol feeding mouse models.Journal of chromatography. B, Analytical technologies in the biomedical and life sciences · 2025
    Article
  10. Review
  11. Article
  12. Article
  13. Article
  14. Article
  15. Article
  16. Article
  17. Article
  18. Alcohol-associated liver disease.The Journal of clinical investigation · 2024
    Review
  19. Experimental In Vivo Toxicity Models for Alcohol Toxicity.The Eurasian journal of medicine · 2023
    Article
  20. Article

28 more citing papers are in PubMed but not listed here.

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

4 authors at 2 institutions in 1 country.

Elizabeth Brandon-WarnerDepartment of Surgery, Carolinas Medical Center, 1000 Blythe Boulevard, Charlotte, NC 28203, USA.
Laura W Schrum
C Max Schmidt
Iain H McKillop
Carolinas Medical Center · USIndiana University – Purdue University Indianapolis · US

Funding

EFFECT OF ALCOHOL ON HEPATOCELLULAR CARCINOMA PROGRESSION IN VIVOR21AA016858 · NIAAA · CAROLINAS MEDICAL CENTER · PI MCKILLOP, IAIN HUGH · 2008 to 2009
$359k
NIAAA NIH HHS AA016858NIAAA NIH HHS R21 AA016858
6 · The paper itself

Abstract

Alcoholic liver disease (ALD) is a major cause of acute and chronic liver disease worldwide. The progressive nature of ALD is well described; however, the complex interactions under which these pathologies evolve remain to be fully elucidated. Clinically there are no clear biomarkers or universally accepted, effective treatment strategies for ALD. Experimental models of ALD are an important component in identifying underlying mechanisms of alcohol-induced injury to develop better diagnostic markers, predictors of disease progression, and therapeutic targets to manage, halt, or reverse disease progression. Rodents remain the most accessible model for studying ALD pathology. Effective rodent models must mimic the natural history of ALD while allowing examination of complex interactions between multiple hepatic, and non-hepatic, cell types in the setting of altered metabolic or oxidative/nitrosative stress, inflammatory responses, and sensitivity to cytotoxic stress. Additionally, mode and duration of alcohol delivery influence hepatic response and present unique challenges in understanding disease pathology. This review provides an overview of rodent models of ALD, their strengths and weaknesses relative to human disease states, and provides insight of the potential to develop novel rodent models to simulate the course of human ALD.

Indexed as

Disease Models, AnimalAlcohol DrinkingAnimalsHumansLiver Diseases, AlcoholicMiceRatsSpecies Specificity

Identifiers

PMID22960051
PMCPMC3496818
OpenAlexW2002511115

What OpenQuestion holds

Textmetadata
LicenceTDM
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.