Evidence map›Paper›PMID 26194645›Full record

ReviewArchives of toxicology2015

Association of Nrf2 with airway pathogenesis: lessons learned from genetic mouse models.

Hye-Youn Cho, Steven R Kleeberger

Open access · bronzeAbstract readReview
In one paragraph

Review in Archives of toxicology, 2015. 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
2.4field-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, 53 citations in OpenAlex.

  1. Review
  2. Persistent exposure to second-hand smoke and asthma endotypes in a study of Puerto Rican youth.Annals of allergy, asthma & immunology : official publication of the American College of Allergy, Asthma, & Immunology · 2026
    Article
  3. Review
  4. Review
  5. Article
  6. Article
  7. Review
  8. Article
  9. Article
  10. Article
  11. Article
  12. The beginning of GPX2 and 30 years later.Free radical biology & medicine · 2022
    Review
  13. Article
  14. Second-hand smoke and NFE2L2 genotype interaction increases paediatric asthma risk and severity.Clinical and experimental allergy : journal of the British Society for Allergy and Clinical Immunology · 2021
    Article
  15. Article
  16. Article
  17. Article
  18. Article
  19. Aurothioglucose enhances proangiogenic pathway activation in lungs from room air and hyperoxia-exposed newborn mice.American journal of physiology. Lung cellular and molecular physiology · 2020
    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 2 institutions in 1 country.

Hye-Youn ChoImmunity, Inflammation, and Diseases Laboratory, National Institute of Environmental Health Sciences, National Institutes of Health, 111 TW Alexander Dr., Building 101, MD D-201, Research Triangle Park, NC, 27709, USA. cho2@niehs.nih.gov.
Steven R KleebergerImmunity, Inflammation, and Diseases Laboratory, National Institute of Environmental Health Sciences, National Institutes of Health, 111 TW Alexander Dr., Building 101, MD D-201, Research Triangle Park, NC, 27709, USA.
National Institute of Environmental Health Sciences · USNational Institutes of Health · US

Funding

The Role Of Nrf2 In Susceptibility To Hyperoxic Lung InjuryZIAES100513 · NIEHS · NATIONAL INSTITUTE OF ENVIRONMENTAL HEALTH SCIENCES · PI KLEEBERGER, STEVEN R · 2009 to 2021
$11.5M
The Role Of Nrf2 In Susceptibility To Hyperoxic Lung InjuryZ01ES100513 · NIEHS · NATIONAL INSTITUTE OF ENVIRONMENTAL HEALTH SCIENCES · PI KLEEBERGER, STEVEN R · 2002 to 2008
$890k
Intramural NIH HHS Z01 ES100513
6 · The paper itself

Abstract

Nrf2 is a key transcription factor for antioxidant response element (ARE)-bearing genes involved in diverse host defense functions including redox balance, cell cycle, immunity, mitochondrial biogenesis, energy metabolism, and carcinogenesis. Nrf2 in the airways is particularly essential as the respiratory system continuously interfaces with environmental stress. Since Nrf2 was determined to be a susceptibility gene for a model of acute lung injury, its protective capacity in the airways has been demonstrated in experimental models of human disorders using Nrf2 mutant mice which were susceptible to supplemental respiratory therapy (e.g., hyperoxia, mechanical ventilation), cigarette smoke, allergens, virus, environmental pollutants, and fibrotic agents compared to wild-type littermates. Recent studies also determined that Nrf2 is indispensable in developmental lung injury. While association studies with genetic NRF2 polymorphisms supported a protective role for murine Nrf2 in oxidative airway diseases, somatic NRF2 mutations enhanced NRF2-ARE responses, and were favorable for lung carcinogenesis and chemoresistance. Bioinformatic tools have elucidated direct Nrf2 targets as well as Nrf2-interacting networks. Moreover, potent Nrf2-ARE agonists protected oxidant-induced lung phenotypes in model systems, suggesting a therapeutic or preventive intervention. Further investigations on Nrf2 should yield greater understanding of its contribution to normal and pathophysiological function in the airways.

Indexed as

Acute Lung InjuryAnimalsAntioxidant Response ElementsComputational BiologyDisease Models, AnimalGenetic Predisposition to DiseaseHumansMiceMice, KnockoutMice, TransgenicNF-E2-Related Factor 2Polymorphism, GeneticRespiratory Tract DiseasesNF-E2-Related Factor 2Antioxidant response elementKnockout miceLungNfe2l2Oxidative stress

Identifiers

PMID26194645
PMCPMC6779142
OpenAlexW2134220633

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.