Evidence map›Paper›PMID 20887622›Full record

ArticleCongestive heart failure (Greenwich, Conn.)

Deciphering STAT3 signaling in the heart: plasticity and vascular inflammation.

Mazen Kurdi, George W Booz

Open access · bronzeAbstract read
In one paragraph

Article in Congestive heart failure (Greenwich, Conn.). The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 12 papers.

0numbers the graph read from it
0cells of the map it votes in
12citing papers in PubMed
1.3field-weighted citation impact, top 18% 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

12 citing papers in PubMed, 21 citations in OpenAlex.

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  2. Aqueous extract ofFrontiers in pharmacology · 2023
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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

2 authors at 1 institution in 2 countries.

Mazen KurdiDepartment of Chemistry and Biochemistry, Lebanese University, Rafic Hariri Educational Campus, Hadath, Lebanon.
George W Booz
University of Mississippi Medical Center · US

Funding

Regulation of IL-6-Type Cytokine Cardioprotective Signaling in the Ischemic HeartR01HL088101 · NHLBI · UNIVERSITY OF MISSISSIPPI MED CTR · PI BOOZ, GEORGE W. · 2008 to 2012
$2.0M
NHLBI NIH HHS 3R01HL088101-02S1NHLBI NIH HHS 5R01HL088101-03NHLBI NIH HHS R01 HL088101
6 · The paper itself

Abstract

Signal transducer and activator of transcription 3 (STAT3) is a transcription factor that plays a critical role in heart development and protection. New developments in understanding its molecular chemistry have revealed the importance of STAT3 in controlling mitochondrial respiration, independent of its function as a transcription factor, and in modulating inflammatory signaling through interactions with other transcription factors and cofactors. The purpose of this article is 2-fold. First, the authors summarize some recent insights into the function of STAT3. Second, the authors seek to illustrate the complexity of targeting a particular cellular protein for therapeutic purposes and the need to consider context when attempting to decipher the role of a particular signaling pathway in the heart. In this case, inflammation, aging, hypertrophy, and heart failure provide new environments that certainly impact on the functioning of STAT3 and on the gene profile linked to its activation.

Indexed as

AnimalsCardiovascular AgentsCoronary DiseaseCytoprotectionDrug DesignHeartHumansHypertrophy, Left VentricularInflammationInterleukin-6MiceMitochondriaModels, AnimalModels, GeneticNeovascularization, PhysiologicPhosphorylationCardiovascular AgentsInterleukin-6STAT3 Transcription FactorSuppressor of Cytokine Signaling Proteins

Identifiers

PMID20887622
PMCPMC2951295
OpenAlexW1623069718

What OpenQuestion holds

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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.