Evidence map›Paper›PMID 30805084›Full record

ArticleOxidative medicine and cellular longevity2019

Thioredoxin Reductase-1 Inhibition Augments Endogenous Glutathione-Dependent Antioxidant Responses in Experimental Bronchopulmonary Dysplasia.

Stephanie B Wall, Rachael Wood, Katelyn Dunigan, Qian Li, Rui Li, Lynette K Rogers, Trent E Tipple

Open access · hybridAbstract read
In one paragraph

Article in Oxidative medicine and cellular longevity, 2019. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 15 papers.

0numbers the graph read from it
0cells of the map it votes in
15citing papers in PubMed
2.0field-weighted citation impact, top 17% 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

15 citing papers in PubMed, 21 citations in OpenAlex.

  1. Article
  2. Molecular Approach of Oxidative Stress and Bronchopulmonary Dysplasia: Relationship of GSTM1 and GSTT1 Genes.Medical principles and practice : international journal of the Kuwait University, Health Science Centre · 2025
    Review
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  5. Preventive Effect ofNutrients · 2023
    Article
  6. Article
  7. Article
  8. Review
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  13. Article
  14. 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
  15. 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

7 authors at 2 institutions in 1 country.

Stephanie B WallNeonatal Redox Biology Laboratory, University of Alabama at Birmingham, Birmingham, AL, USA.
Rachael WoodNeonatal Redox Biology Laboratory, University of Alabama at Birmingham, Birmingham, AL, USA.
Katelyn DuniganNeonatal Redox Biology Laboratory, University of Alabama at Birmingham, Birmingham, AL, USA.
Qian LiNeonatal Redox Biology Laboratory, University of Alabama at Birmingham, Birmingham, AL, USA.
Rui LiNeonatal Redox Biology Laboratory, University of Alabama at Birmingham, Birmingham, AL, USA.
Lynette K RogersCenter for Perinatal Research, The Research Institute at Nationwide Children's Hospital, Columbus, OH, USA.ORCID 0000-0003-3413-5379
Trent E TippleNeonatal Redox Biology Laboratory, University of Alabama at Birmingham, Birmingham, AL, USA.ORCID 0000-0002-5156-4282
University of Alabama at Birmingham · USNationwide Children's Hospital · US

Funding

Targeting Thioredoxin Reductase-1 to Prevent Bronchopulmonary DysplasiaR01HL119280 · NHLBI · UNIVERSITY OF ALABAMA AT BIRMINGHAM · PI TIPPLE, TRENT · 2014 to 2018
$2.0M
NHLBI NIH HHS R01 HL119280
6 · The paper itself

Abstract

backgroundAurothioglucose- (ATG-) mediated inhibition of thioredoxin reductase-1 (TXNRD1) improves alveolarization in experimental murine bronchopulmonary dysplasia (BPD). Glutathione (GSH) mediates susceptibility to neonatal and adult oxidative lung injury. We have previously shown that ATG attenuates hyperoxic lung injury and enhances glutathione- (GSH-) dependent antioxidant defenses in adult mice. HYPOTHESIS: The present studies evaluated the effects of TXNRD1 inhibition on GSH-dependent antioxidant defenses in newborn mice

methodsNewborn mice received intraperitoneal ATG or saline prior to room air or 85% hyperoxia exposure. Glutamate-cysteine ligase (GCL) catalytic (Gclc) and modifier (Gclm) mRNA levels, total GSH levels, total GSH peroxidase (GPx) activity, and Gpx2 expression were determined in lung homogenates.

results

conclusionsOur data are consistent with a model in which TXNRD1 inhibition augments hyperoxia-induced GSH-dependent antioxidant responses in neonatal mice. Discrepancies between

Indexed as

AnimalsAnimals, NewbornAntioxidantsAurothioglucoseBronchopulmonary DysplasiaEpithelial CellsGlutamate-Cysteine LigaseGlutathioneGlutathione PeroxidaseHyperoxiaLungMiceRNA, MessengerThioredoxin Reductase 1AntioxidantsAurothioglucoseGlutamate-Cysteine LigaseGlutathioneGlutathione PeroxidaseRNA, MessengerThioredoxin Reductase 1

Identifiers

PMID30805084
PMCPMC6360549
OpenAlexW2910112716

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.