Evidence map›Paper›PMID 21252049›Full record

ReviewAmerican journal of physiology. Gastrointestinal and liver physiology2011

Innate immunity in alcoholic liver disease.

Bin Gao, Ekihiro Seki, David A Brenner, Scott Friedman, Jessica I Cohen, Laura Nagy, Gyongyi Szabo, Samir Zakhari

Abstract readReview
In one paragraph

Review in American journal of physiology. Gastrointestinal and liver physiology, 2011. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 139 papers.

0numbers the graph read from it
0cells of the map it votes in
139citing 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

139 citing papers in PubMed, 221 citations in OpenAlex.

  1. Article
  2. Review
  3. Review
  4. Article
  5. Review
  6. 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
  7. Synergistic toxicity in alcohol-associated liver disease and PFAS exposure.Toxicological sciences : an official journal of the Society of Toxicology · 2025
    Review
  8. Article
  9. Review
  10. Review
  11. Article
  12. Review
  13. Review
  14. Liver Cirrhosis: The Immunocompromised State.Journal of clinical medicine · 2024
    Review
  15. Targeting cAMP signaling and phosphodiesterase 4 for liver disease treatment.Medicinal chemistry research : an international journal for rapid communications on design and mechanisms of action of biologically active agents · 2024
    Article
  16. The Role of Interferon Regulatory Factors in Liver Diseases.International journal of molecular sciences · 2024
    Review
  17. Review
  18. Article
  19. Article
  20. Article

79 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

8 authors at 5 institutions in 1 country.

Bin GaoLaboratory of Liver Diseases, National Institute on Alcohol Abuse and Alcoholism, National Institutes of Health, Bethesda, Maryland 20892, USA. bgao@mail.nih.gov
Ekihiro Seki
David A Brenner
Scott Friedman
Jessica I Cohen
Laura Nagy
Gyongyi Szabo
Samir Zakhari
Cleveland Clinic · USUniversity of California, San Diego · USIcahn School of Medicine at Mount Sinai · USNational Institutes of Health · USUniversity of Massachusetts Chan Medical School · US

Funding

LPS binding to TLR4 regulates hepatic stellate cell activation and fibrosisR01DK085252 · NIDDK · UNIVERSITY OF CALIFORNIA, SAN DIEGO · PI EKIHIRO SEKI · 2011 to 2026
$4.8M
TNF ALPHA AND IMPAIRED WOUND HEALING OF CACHEXIA XIAR01GM041804 · NIGMS · UNIVERSITY OF NORTH CAROLINA CHAPEL HILL · PI BRENNER, DAVID A. · 1989 to 2013
$3.4M
Synergistic Actions By Multiple Toll-Like Receptors in Alcoholic Liver DiseaseR01AA020172 · NIAAA · UNIVERSITY OF CALIFORNIA, SAN DIEGO · PI SEKI, EKIHIRO · 2010 to 2014
$1.8M
NIAAA NIH HHS R01 AA020172NIDDK NIH HHS R01 DK085252NIGMS NIH HHS R01 GM041804
6 · The paper itself

Abstract

Excessive alcohol consumption is a leading cause of chronic liver disease in the Western world. Alcohol-induced hepatotoxicity and oxidative stress are important mechanisms contributing to the pathogenesis of alcoholic liver disease. However, emerging evidence suggests that activation of innate immunity involving TLR4 and complement also plays an important role in initiating alcoholic steatohepatitis and fibrosis, but the role of adaptive immunity in the pathogenesis of alcoholic liver disease remains obscure. Activation of a TLR4-mediated MyD88-independent (TRIF/IRF-3) signaling pathway in Kupffer cells contributes to alcoholic steatohepatitis, whereas activation of TLR4 signaling in hepatic stellate cells promotes liver fibrosis. Alcohol consumption activates the complement system in the liver by yet unidentified mechanisms, leading to alcoholic steatohepatitis. In contrast to activation of TLR4 and complement, alcohol consumption can inhibit natural killer cells, another important innate immunity component, contributing to alcohol-mediated acceleration of viral infection and liver fibrosis in patients with chronic viral hepatitis. Understanding of the role of innate immunity in the pathogenesis of alcoholic liver disease may help us identify novel therapeutic targets to treat this disease.

Indexed as

HumansImmunity, InnateKiller Cells, NaturalKupffer CellsLiverLiver Diseases, AlcoholicSignal TransductionToll-Like Receptor 4Toll-Like Receptor 4

Identifiers

PMID21252049
PMCPMC3774265
OpenAlexW2163224810

What OpenQuestion holds

Textmetadata
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.