Evidence map›Paper›PMID 30212802›Full record

ArticleRedox biology2018

Selenium supplementation of lung epithelial cells enhances nuclear factor E2-related factor 2 (Nrf2) activation following thioredoxin reductase inhibition.

Rachael Tindell, Stephanie B Wall, Qian Li, Rui Li, Katelyn Dunigan, Rachael Wood, Trent E Tipple

Registry-linked trialOpen access · goldAbstract read
In one paragraph

Article in Redox biology, 2018. The graph could read no effect estimate from its abstract, so it casts no vote on the map. It is linked to trial NCT04869579 (Selenium as a Potential Treatment for Moderately-ill, Severely-ill, and Critically-ill COVID-19 Patients), which is not on this map. Cited by 16 papers.

0numbers the graph read from it
0cells of the map it votes in
16citing papers in PubMed
1.8field-weighted citation impact, top 16% 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.

NCT04869579 phase2unknown statusnot on this mapstarted 2021, after this paper: background citation

Selenium as a Potential Treatment for Moderately-ill, Severely-ill, and Critically-ill COVID-19 Patients

TypeinterventionalSponsorCHRISTUS HealthRan2021 to 2021Enrolled100ConditionsCovid19ArmsSelenium (as Selenious Acid), Placebo
3 · Its place in the literature

Who cites it

16 citing papers in PubMed, 30 citations in OpenAlex.

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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 1 institution in 1 country.

Rachael TindellNeonatal Redox Biology Laboratory, University of Alabama at Birmingham, Birmingham, AL, USA; Department of Pediatrics, University of Alabama at Birmingham, Birmingham, AL, USA.
Stephanie B WallNeonatal Redox Biology Laboratory, University of Alabama at Birmingham, Birmingham, AL, USA; Department of Pediatrics, University of Alabama at Birmingham, Birmingham, AL, USA.
Qian LiNeonatal Redox Biology Laboratory, University of Alabama at Birmingham, Birmingham, AL, USA; Department of Pediatrics, University of Alabama at Birmingham, Birmingham, AL, USA.
Rui LiNeonatal Redox Biology Laboratory, University of Alabama at Birmingham, Birmingham, AL, USA; Department of Pediatrics, University of Alabama at Birmingham, Birmingham, AL, USA.
Katelyn DuniganNeonatal Redox Biology Laboratory, University of Alabama at Birmingham, Birmingham, AL, USA; Department of Pediatrics, University of Alabama at Birmingham, Birmingham, AL, USA.
Rachael WoodNeonatal Redox Biology Laboratory, University of Alabama at Birmingham, Birmingham, AL, USA.
Trent E TippleNeonatal Redox Biology Laboratory, University of Alabama at Birmingham, Birmingham, AL, USA; Department of Pediatrics, University of Alabama at Birmingham, Birmingham, AL, USA. Electronic address: ttipple@peds.uab.edu.
University of Alabama at Birmingham · 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

The trace element selenium (Se) contributes to redox signaling, antioxidant defense, and immune responses in critically ill neonatal and adult patients. Se is required for the synthesis and function of selenoenzymes including thioredoxin (Trx) reductase-1 (TXNRD1) and glutathione peroxidases (GPx). We have previously identified TXNRD1, primarily expressed by airway epithelia, as a promising therapeutic target to prevent lung injury, likely via nuclear factor E2-related factor 2 (Nrf2)-dependent mechanisms. The present studies utilized the TXNRD1 inhibitor auranofin (AFN) to test the hypothesis that Se positively influences Nrf2 activation and selenoenzyme responses in lung epithelial cells. Murine transformed Club cells (mtCCs) were supplemented with 0, 10, 25, or 100 nM Na

Indexed as

AnimalsCell LineEpithelial CellsGlutathione PeroxidaseLungMiceNF-E2-Related Factor 2Respiratory MucosaSeleniumThioredoxin Reductase 1Glutathione PeroxidaseGpx2 protein, mouseNfe2l2 protein, mouseNF-E2-Related Factor 2SeleniumThioredoxin Reductase 1Txnrd1 protein, mouse

Identifiers

PMID30212802
PMCPMC6134185
OpenAlexW2890716110

What OpenQuestion holds

Textmetadata
LicenceCC BY-NC-ND
Read underepoch 390

Registered trials

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.