Evidence map›Paper›PMID 19450559›Full record

ArticleBiochemical and biophysical research communications2009

STAT3 deletion sensitizes cells to oxidative stress.

Seán P Barry, Paul A Townsend, James McCormick, Richard A Knight, Tiziano M Scarabelli, David S Latchman, Anastasis Stephanou

Open access · hybridAbstract read
In one paragraph

Article in Biochemical and biophysical research communications, 2009. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 35 papers.

0numbers the graph read from it
0cells of the map it votes in
35citing papers in PubMed
1.9field-weighted citation impact, top 14% 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

35 citing papers in PubMed, 64 citations in OpenAlex.

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  15. Redox Regulation of STAT1 and STAT3 Signaling.International journal of molecular sciences · 2020
    Review
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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 3 institutions in 2 countries.

Seán P BarryMedical Molecular Biology Unit, Institute of Child Health, University College London, 30 Guilford Street, London WC1N1EH, UK.
Paul A Townsend
James McCormick
Richard A Knight
Tiziano M Scarabelli
David S Latchman
Anastasis Stephanou
University College London · GBSouthampton General Hospital · GBSt. John Hospital & Medical Center · US

Funding

British Heart Foundation
6 · The paper itself

Abstract

The transcription factor STAT1 plays a role in promoting apoptotic cell death, whereas the related STAT3 transcription factor protects cardiac myocytes from ischemia/reperfusion (I/R) injury or oxidative stress. Cytokines belonging to the IL-6 family activate the JAK-STAT3 pathway, but also activate other cytoprotective pathways such as the MAPK-ERK or the PI3-AKT pathway. It is therefore unclear whether STAT3 is the only cytoprotective mediator against oxidative stress-induced cell death. Overexpression of STAT3 in primary neonatal rat ventricular myocytes (NRVM) protects against I/R-induced cell death. Moreover, a dominant negative STAT3 adenovirus (Ad ST3-DN) enhanced apoptotic cell death (81.2+/-6.9%) compared to control infected NRVM (46.0+/-3.1%) following I/R. Depletion of STAT3 sensitized cells to apoptotic cell death following oxidative stress. These results provide direct evidence for the role of STAT3 as a cytoprotective transcription factor in cells exposed to oxidative stress.

Indexed as

AnimalsApoptosisCell LineGene DeletionMiceMutationMyocardial Reperfusion InjuryMyocytes, CardiacOxidative StressRatsSTAT3 Transcription FactorSTAT3 Transcription Factor

Identifiers

PMID19450559
PMCPMC2706948
OpenAlexW2072255457

What OpenQuestion holds

Textmetadata
LicenceCC BY-NC-ND
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.