Evidence map›Paper›PMID 22524187›Full record

ReviewAnnual review of nutrition2012

Inflammation in alcoholic liver disease.

H Joe Wang, Bin Gao, Samir Zakhari, Laura E Nagy

Abstract readReview
In one paragraph

Review in Annual review of nutrition, 2012. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 158 papers.

0numbers the graph read from it
0cells of the map it votes in
158citing papers in PubMed
13.7field-weighted citation impact, top 1% 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

158 citing papers in PubMed, 293 citations in OpenAlex.

  1. Trial
  2. Article
  3. International journal of molecular sciences · 2026
    Article
  4. Observational
  5. Article
  6. Article
  7. Review
  8. Article
  9. Review
  10. Article
  11. Identification of an IRF-ZBP1-caspase-8-NINJ1 axis in driving PANoptosis and pathology during alcohol-associated liver disease.Proceedings of the National Academy of Sciences of the United States of America · 2025
    Article
  12. Synergistic toxicity in alcohol-associated liver disease and PFAS exposure.Toxicological sciences : an official journal of the Society of Toxicology · 2025
    Review
  13. Article
  14. Article
  15. Review
  16. Article
  17. Article
  18. Article
  19. Article
  20. Review

98 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 4 institutions in 1 country.

H Joe WangDivision of Metabolism and Health Effects, National Institute on Alcohol Abuse and Alcoholism, Bethesda, Maryland 20892, USA. wangh4@mail.nih.gov
Bin Gao
Samir Zakhari
Laura E Nagy
Case Western Reserve University · USHealth Effects Institute · USNational Cancer Institute · USNational Institute on Alcohol Abuse and Alcoholism · US

Funding

Pathogenesis and Novel Therapeutic Targets of Steatotic Liver Disease and CancerZIAAA000369 · NIAAA · NATIONAL INSTITUTE ON ALCOHOL ABUSE AND ALCOHOLISM · PI GAO, BIN · 2009 to 2025
$23.4M
Molecular mechanisms of liver injury, repair, and immunityZIAAA000368 · NIAAA · NATIONAL INSTITUTE ON ALCOHOL ABUSE AND ALCOHOLISM · PI GAO, BIN · 2009 to 2023
$16.1M
ETHANOL REGULATION OF KUPFFER CELL SIGNAL TRANSDUCTIONR01AA011975 · NIAAA · CLEVELAND CLINIC LERNER COM-CWRU · PI NAGY, LAURA E. · 1999 to 2014
$4.1M
Role of Adipose in Ethanol-Induced Tissue InjuryR37AA011876 · NIAAA · CLEVELAND CLINIC LERNER COM-CWRU · PI NAGY, LAURA E. · 2009 to 2018
$4.0M
INSULIN MEDIATED GLUCOSE TRANSPORT DISRUPT BY ETHANOLR01AA011876 · NIAAA · CLEVELAND CLINIC LERNER COM-CWRU · PI NAGY, LAURA E · 1998 to 2007
$2.4M
Pilot ProjectP20AA017837 · NIAAA · CLEVELAND CLINIC LERNER COM-CWRU · PI NAGY, LAURA E. · 2009 to 2013
$2.2M
Complement and ethanol-induced liver injury.R01AA016399 · NIAAA · CLEVELAND CLINIC LERNER COM-CWRU · PI NAGY, LAURA E. · 2006 to 2010
$1.7M
Intramural NIH HHS Z99 AA999999Intramural NIH HHS ZIA AA000368Intramural NIH HHS ZIA AA000369NIAAA NIH HHS P20 AA017837NIAAA NIH HHS R01 AA011876NIAAA NIH HHS R01 AA011975NIAAA NIH HHS R01 AA016399NIAAA NIH HHS R37 AA011876
6 · The paper itself

Abstract

Frank Burr Mallory's landmark observation in 1911 on the histopathology of alcoholic liver disease (ALD) was the first identification of a link between inflammation and ALD. In this review, we summarize recent advances regarding the origins and roles of various inflammatory components in ALD. Metabolism of ethanol generates a number of metabolites, including acetate, reactive oxygen species, acetaldehyde, and epigenetic changes, that can induce inflammatory responses. Alcohol and its metabolites can also initiate and aggravate inflammatory conditions by promoting gut leakiness of microbial products, by sensitizing immune cells to stimulation, and by activating innate immune pathways, such as complement. Chronic alcohol consumption also sensitizes nonimmune cells, e.g., hepatocytes, to inflammatory signals and impairs their ability to respond to protective signals. Based on these advances, a number of inflammatory targets have been identified with potential for therapeutic intervention in ALD, presenting new opportunities and challenges for translational research.

Indexed as

AnimalsAntioxidantsHumansImmune SystemImmunologic FactorsInflammation MediatorsLiver Diseases, AlcoholicAntioxidantsImmunologic FactorsInflammation Mediators

Identifiers

PMID22524187
PMCPMC3670145
OpenAlexW2114405620

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.