Evidence map›Paper›PMID 23346021›Full record

ArticleTheScientificWorldJournal2012

Chronic-alcohol-abuse-induced oxidative stress in the development of acute respiratory distress syndrome.

Yan Liang, Samantha M Yeligar, Lou Ann S Brown

Open access · goldAbstract read
In one paragraph

Article in TheScientificWorldJournal, 2012. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 37 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
37citing papers in PubMed, 1 pooled it
2.6field-weighted citation impact, top 11% 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

37 citing papers in PubMed, 1 synthesis or guideline pooled it, 55 citations in OpenAlex.

  1. Alcohol's Effects on the Lung and Lung Disease.Alcohol research : current reviews · 2025
    Pooled it
  2. Trial
  3. Article
  4. The association between alcohol consumption and pulmonary function: a scoping review.European respiratory review : an official journal of the European Respiratory Society · 2024
    Article
  5. Article
  6. Review
  7. Article
  8. Article
  9. Review
  10. Review
  11. Article
  12. Review
  13. Review
  14. Article
  15. Article
  16. Article
  17. The role of cytochrome P450 (CYP) enzymes in hyperoxic lung injury.Expert opinion on drug metabolism & toxicology · 2021
    Review
  18. Article
  19. Innate Immunity and Alcohol.Journal of clinical medicine · 2019
    Review
  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.

Yan LiangDivision of Neonatal-Perinatal Medicine, Department of Pediatrics, Emory University and Children's Healthcare of Atlanta Center for Developmental Lung Biology, Atlanta, GA 30322, USA.
Samantha M Yeligar
Lou Ann S Brown
Children's Healthcare of Atlanta · US

Funding

Institutional Training Grant in Alcohol ResearchT32AA013528 · NIAAA · EMORY UNIVERSITY · PI GUIDOT, DAVID MARSHALL · 2002 to 2011
$3.2M
NIAAA NIH HHS 1P50AA135757NIAAA NIH HHS 5T32AA013528NIAAA NIH HHS T32 AA013528PHS HHS 5R01 012197
6 · The paper itself

Abstract

Chronic alcohol ingestion increases the risk of developing acute respiratory distress syndrome (ARDS), a severe form of acute lung injury, characterized by alveolar epithelial and endothelial barrier disruption and intense inflammation. Alcohol abuse is also associated with a higher incidence of sepsis or pneumonia resulting in a higher rate of admittance to intensive care, longer inpatient stays, higher healthcare costs, and a 2-4 times greater mortality rate. Chronic alcohol ingestion induced severe oxidative stress associated with increased ROS generation, depletion of the critical antioxidant glutathione (GSH), and oxidation of the thiol/disulfide redox potential in the alveolar epithelial lining fluid and exhaled breath condensate. Across intracellular and extracellular GSH pools in alveolar type II cells and alveolar macrophages, chronic alcohol ingestion consistently induced a 40-60 mV oxidation of GSH/GSSG suggesting that the redox potentials of different alveolar GSH pools are in equilibrium. Alcohol-induced GSH depletion or oxidation was associated with impaired functions of alveolar type II cells and alveolar macrophages but could be reversed by restoring GSH pools in the alveolar lining fluid. The aims of this paper are to address the mechanisms for alcohol-induced GSH depletion and oxidation and the subsequent effects in alveolar barrier integrity, modulation of the immune response, and apoptosis.

Indexed as

Alcohol DrinkingAlcoholismApoptosisChronic DiseaseDisulfidesGlutathioneHumansLungMacrophages, AlveolarMitochondriaOxidation-ReductionOxidative StressPulmonary AlveoliReactive Oxygen SpeciesRespiratory Distress SyndromeSulfhydryl CompoundsDisulfidesGlutathioneReactive Oxygen SpeciesSulfhydryl Compounds

Identifiers

PMID23346021
PMCPMC3543796
OpenAlexW2024681990

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.