Evidence map›Paper›PMID 21126203›Full record

ReviewAntioxidants & redox signaling2011

Redox signaling and the innate immune system in alcoholic liver disease.

Jessica I Cohen, Xiaocong Chen, Laura E Nagy

Abstract readReview
In one paragraph

Review in Antioxidants & redox signaling, 2011. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 40 papers.

0numbers the graph read from it
0cells of the map it votes in
40citing papers in PubMed
3.9field-weighted citation impact, top 6% 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

40 citing papers in PubMed, 68 citations in OpenAlex.

  1. Article
  2. Article
  3. Review
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  6. Review
  7. Review
  8. Article
  9. Article
  10. Article
  11. Redox Control of the Immune Response in the Hepatic Progenitor Cell Niche.Frontiers in cell and developmental biology · 2020
    Article
  12. Article
  13. Article
  14. Alcohol Consumption Can be a "Double-Edged Sword" for Chronic Kidney Disease Patients.Medical science monitor : international medical journal of experimental and clinical research · 2019
    Review
  15. Review
  16. Article
  17. Review
  18. Review
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  20. Article
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

3 authors at 1 institution in 1 country.

Jessica I CohenDepartment of Pathobiology, Cleveland Clinic, Cleveland, Ohio 44195, USA.
Xiaocong Chen
Laura E Nagy
Cleveland Clinic · US

Funding

ETHANOL REGULATION OF KUPFFER CELL SIGNAL TRANSDUCTIONR01AA011975 · NIAAA · CLEVELAND CLINIC LERNER COM-CWRU · PI NAGY, LAURA E. · 1999 to 2014
$4.1M
Complement and ethanol-induced liver injury.R01AA016399 · NIAAA · CLEVELAND CLINIC LERNER COM-CWRU · PI NAGY, LAURA E. · 2006 to 2010
$1.7M
Thioredoxin and ethanol-induced liver injuryF31AA016434 · NIAAA · CLEVELAND CLINIC LERNER COM-CWRU · PI COHEN, JESSICA · 2006 to 2009
$92k
NIAAA NIH HHS F31 AA016434NIAAA NIH HHS P20AA017069NIAAA NIH HHS R01AA11975NIAAA NIH HHS R01AA16399
6 · The paper itself

Abstract

The development of alcoholic liver disease (ALD) is a complex process involving both parenchymal and nonparenchymal cells resident in the liver. Although the mechanisms for ALD are not completely understood, it is clear that increased oxidative stress, and activation of the innate immune system are essential elements in the pathophysiology of ALD. Oxidative stress from ethanol exposure results from increased generation of reactive oxygen species and decreased hepatocellular antioxidant activity, including changes in the thioredoxin/peroxiredoxin family of proteins. Both cellular and circulating components of the innate immune system are activated by exposure to ethanol. For example, ethanol exposure enhances toll-like receptor-4 (TLR-4)-dependent cytokine expression by Kupffer cells, likely due, at least in part, to dysregulation of redox signaling. Similarly, complement activation in response to ethanol leads to increased production of the anaphylatoxins, C3a and C5a, and activation C3a receptor and C5a receptor. Complement activation thus contributes to increased inflammatory cytokine production and can influence redox signaling. Here we will review recent progress in understanding the interactions between oxidative stress and innate immunity in ALD. These data illustrate that ethanol-induced oxidative stress and activation of the innate immune system interact dynamically during ethanol exposure, exacerbating ethanol-induced liver injury.

Indexed as

Immunity, InnateSignal TransductionLiver Diseases, AlcoholicOxidation-ReductionReactive Oxygen SpeciesReactive Oxygen Species

Identifiers

PMID21126203
PMCPMC3118704
OpenAlexW2029578496

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.