Evidence map›Paper›PMID 22683820›Full record

ReviewFree radical biology & medicine2012

Role of GSTM1 in resistance to lung inflammation.

Weidong Wu, David Peden, David Diaz-Sanchez

Open access · greenAbstract readReview
In one paragraph

Review in Free radical biology & medicine, 2012. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 20 papers.

0numbers the graph read from it
0cells of the map it votes in
20citing papers in PubMed
1.5field-weighted citation impact, top 19% 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

20 citing papers in PubMed, 45 citations in OpenAlex.

  1. Trial
  2. Changes in Metabolites Present in Lung-Lining Fluid Following Exposure of Humans to Ozone.Toxicological sciences : an official journal of the Society of Toxicology · 2018
    Trial
  3. Review
  4. Article
  5. Article
  6. Article
  7. Review
  8. Article
  9. Review
  10. Review
  11. Frontiers in molecular biosciences · 2021
    Article
  12. Article
  13. Air pollutants and early origins of respiratory diseases.Chronic diseases and translational medicine · 2018
    Article
  14. Article
  15. Children's Inter-Individual Variability and Asthma Development.International journal of health sciences · 2015
    Review
  16. Environmental effects on immune responses in patients with atopy and asthma.The Journal of allergy and clinical immunology · 2014
    Review
  17. Inflammasome Activity in Non-Microbial Lung Inflammation.Journal of environmental immunology and toxicology · 2014
    Article
  18. Review
  19. PM2.5, oxidant defence and cardiorespiratory health: a review.Environmental health : a global access science source · 2013
    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 2 institutions in 1 country.

Weidong WuDepartment of Pediatrics, Center for Environmental Medicine, Asthma, and Lung Biology, University of North Carolina, Chapel Hill, NC 7599, USA. Weidong_Wu@med.unc.edu
David Peden
David Diaz-Sanchez
University of North Carolina at Chapel Hill · USEnvironmental Protection Agency · US

Funding

P2X7 and the Inflammasome Pathways in Lung InflammationU19AI077437 · NIAID · UNIV OF NORTH CAROLINA CHAPEL HILL · PI PEDEN, DAVID B. · 2008 to 2013
$9.2M
Childhood Asthma, Susceptibility and Biological Activity of Ambient ParticlesR01ES016535 · NIEHS · UNIVERSITY OF SOUTHERN CALIFORNIA · PI MCCONNELL, ROB S · 2008 to 2011
$2.0M
NIAID NIH HHS U19 AI077437NIAID NIH HHS U19AI077437NIEHS NIH HHS R01 ES016535NIEHS NIH HHS R01ES016535
6 · The paper itself

Abstract

Lung inflammation resulting from oxidant/antioxidant imbalance is a common feature of many lung diseases. In particular, the role of enzymes regulated by the NF-E2-related factor 2 transcription factor has recently received increased attention. Among these antioxidant genes, glutathione S-transferase Mu 1 (GSTM1) has been most extensively characterized because it has a null polymorphism that is highly prevalent in the population and associated with increased risk of inflammatory lung diseases. Present evidence suggests that GSTM1 acts through interactions with other genes and environmental factors, especially air pollutants. Here, we review GSTM1 gene expression and regulation and summarize the findings from epidemiological, clinical, animal, and in vitro studies on the role played by GSTM1 in lung inflammation. We discuss limitations in the existing knowledge base and future perspectives and evaluate the potential of pharmacologic and genetic manipulation of the GSTM1 gene to modulate pulmonary inflammatory responses.

Indexed as

Air PollutionAnimalsAntioxidantsGene ExpressionGlutathione TransferaseHumansOxidative StressPneumoniaSequence DeletionAntioxidantsGlutathione Transferase

Identifiers

PMID22683820
PMCPMC3418458
OpenAlexW2002681738

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.