Evidence map›Paper›PMID 23892124›Full record

ReviewToxicology letters2013

Alcoholic lung injury: metabolic, biochemical and immunological aspects.

Lata Kaphalia, William J Calhoun

Open access · hybridAbstract readReview
In one paragraph

Review in Toxicology letters, 2013. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 49 papers, 2 of them syntheses that pooled it.

0numbers the graph read from it
0cells of the map it votes in
49citing papers in PubMed, 2 pooled it
7.3field-weighted citation impact, top 2% 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

49 citing papers in PubMed, 2 syntheses or guidelines pooled it, 103 citations in OpenAlex.

  1. Pooled it
  2. Alcohol's Effects on the Lung and Lung Disease.Alcohol research : current reviews · 2025
    Pooled it
  3. Article
  4. Article
  5. Review
  6. Review
  7. Article
  8. Article
  9. Review
  10. Review
  11. Article
  12. Article
  13. Oxidative stress in Wernicke's encephalopathy.Frontiers in aging neuroscience · 2023
    Review
  14. Review
  15. Article
  16. Review
  17. Article
  18. Review
  19. Article
  20. Review
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

2 authors at 1 institution in 1 country.

Lata KaphaliaDivision of Pulmonary, Allergy, and Critical Care Medicine, Department of Medicine, University of Texas Medical Branch, Galveston, TX, United States.
William J Calhoun
The University of Texas Medical Branch at Galveston · US

Funding

UTMB CLINICAL AND TRANSLATIONAL SCIENCE AWARD: NASA BED REST STUDIESUL1RR029876 · NCRR · UNIVERSITY OF TEXAS MED BR GALVESTON · PI BRASIER, ALLAN R. · 2009 to 2011
$17.7M
NCRR NIH HHS UL1 RR029876
6 · The paper itself

Abstract

Chronic alcohol abuse is a systemic disorder and a risk factor for acute respiratory distress syndrome (ARDS) and chronic obstructive pulmonary disease (COPD). A significant amount of ingested alcohol reaches airway passages in the lungs and can be metabolized via oxidative and non-oxidative pathways. About 90% of the ingested alcohol is metabolized via hepatic alcohol dehydrogenase (ADH)-catalyzed oxidative pathway. Alcohol can also be metabolized by cytochrome P450 2E1 (CYP2E1), particularly during chronic alcohol abuse. Both the oxidative pathways, however, are associated with oxidative stress due to the formation of acetaldehyde and/or reactive oxygen species (ROS). Alcohol ingestion is also known to cause endoplasmic reticulum (ER) stress, which can be mediated by oxidative and/or non-oxidative metabolites of ethanol. An acute as well as chronic alcohol ingestions impair protective antioxidants, oxidize reduced glutathione (GSH, cellular antioxidant against ROS and oxidative stress), and suppress innate and adaptive immunity in the lungs. Oxidative stress and suppressed immunity in the lungs of chronic alcohol abusers collectively are considered to be major risk factors for infection and development of pneumonia, and such diseases as ARDS and COPD. Prior human and experimental studies attempted to identify common mechanisms by which alcohol abuse directly causes toxicity to alveolar epithelium and respiratory tract, particularly lungs. In this review, the metabolic basis of lung injury, oxidative and ER stress and immunosuppression in experimental models and alcoholic patients, as well as potential immunomodulatory therapeutic strategies for improving host defenses against alcohol-induced pulmonary infections are discussed.

Indexed as

Adaptive ImmunityAlcoholismAnimalsEndoplasmic Reticulum StressHumansImmunity, InnateImmunocompromised HostLungOxidative StressPulmonary Disease, Chronic ObstructiveRespiratory Distress SyndromeRespiratory MucosaRespiratory SystemRisk FactorsER stressEthanolLungMetabolismOxidative stress

Identifiers

PMID23892124
PMCPMC3806189
OpenAlexW2002591374

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.