Evidence map›Paper›PMID 22675432›Full record

ArticlePloS one2012

Acrolein induces endoplasmic reticulum stress and causes airspace enlargement.

Yoshiaki Kitaguchi, Laimute Taraseviciene-Stewart, Masayuki Hanaoka, Ramesh Natarajan, Donatas Kraskauskas, Norbert F Voelkel

Open access · goldAbstract read
In one paragraph

Article in PloS one, 2012. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 33 papers.

0numbers the graph read from it
0cells of the map it votes in
33citing papers in PubMed
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

33 citing papers in PubMed, 62 citations in OpenAlex.

  1. Article
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  7. Environmental neurotoxic pollutants: review.Environmental science and pollution research international · 2020
    Review
  8. CFTR targeted therapies: recent advances in cystic fibrosis and possibilities in other diseases of the airways.European respiratory review : an official journal of the European Respiratory Society · 2020
    Review
  9. Review
  10. Review
  11. Article
  12. Observational
  13. Effects of cigarette smoke on pulmonary endothelial cells.American journal of physiology. Lung cellular and molecular physiology · 2018
    Review
  14. Article
  15. Alda-1 Protects Against Acrolein-Induced Acute Lung Injury and Endothelial Barrier Dysfunction.American journal of respiratory cell and molecular biology · 2017
    Article
  16. Article
  17. Article
  18. Oxidative medicine and cellular longevity · 2017
    Article
  19. 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

6 authors at 2 institutions in 1 country.

Yoshiaki KitaguchiPulmonary and Critical Care Medicine Division, The Victoria Johnson Laboratory for Obstructive Lung Disease Research, Virginia Commonwealth University, Richmond, Virginia, United States of America.
Laimute Taraseviciene-Stewart
Masayuki Hanaoka
Ramesh Natarajan
Donatas Kraskauskas
Norbert F Voelkel
Virginia Commonwealth University · USUniversity of Colorado Denver · US

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

backgroundGiven the relative abundance and toxic potential of acrolein in inhaled cigarette smoke, it is surprising how little is known about the pulmonary and systemic effects of acrolein. Here we test the hypothesis whether systemic administration of acrolein could cause endoplasmic reticulum (ER) stress, and lung cell apoptosis, leading to the enlargement of the alveolar air spaces in rats.

methodsAcute and chronic effects of intraperitoneally administered acrolein were tested. Mean alveolar airspace area was measured by using light microscopy and imaging system software. TUNEL staining and immunohistochemistry (IHC) for active caspase 3 and Western blot analysis for active caspase 3, and caspase 12 were performed to detect apoptosis. The ER-stress related gene expression in the lungs was determined by Quantitative real-time PCR analysis. Acrolein-protein adducts in the lung tissue were detected by IHC.

resultsAcute administration of acrolein caused a significant elevation of activated caspase 3, upregulation of VEGF expression and induced ER stress proteins in the lung tissue. The chronic administration of acrolein in rats led to emphysematous lung tissue remodeling. TUNEL staining and IHC for cleaved caspase 3 showed a large number of apoptotic septal cells in the acrolein-treated rat lungs. Chronic acrolein administration cause the endoplasmic reticulum stress response manifested by significant upregulation of ATF4, CHOP and GADd34 expression. In smokers with COPD there was a considerable accumulation of acrolein-protein adducts in the inflammatory, airway and vascular cells.

conclusionsSystemic administration of acrolein causes endoplasmic reticulum stress response, lung cell apoptosis, and chronic administration leads to the enlargement of the alveolar air spaces and emphysema in rats. The substantial accumulation of acrolein-protein adducts in the lungs of COPD patients suggest a role of acrolein in the pathogenesis of emphysema.

Indexed as

AcroleinAnimalsCaspase 3Endoplasmic Reticulum StressGene ExpressionLungMaleProtein BindingPulmonary Disease, Chronic ObstructivePulmonary EmphysemaRatsRats, Sprague-DawleyUnfolded Protein ResponseVascular Endothelial Growth Factor AAcroleinCaspase 3Vascular Endothelial Growth Factor A

Identifiers

PMID22675432
PMCPMC3364999
OpenAlexW2025620259

What OpenQuestion holds

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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.