Evidence map›Paper›PMID 24069556›Full record

ReviewJAK-STAT2013

Dancing rhinos in stilettos: The amazing saga of the genomic and nongenomic actions of STAT3 in the heart.

Fouad A Zouein, Mazen Kurdi, George W Booz

Open access · bronzeAbstract readReview
In one paragraph

Review in JAK-STAT, 2013. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 21 papers.

0numbers the graph read from it
0cells of the map it votes in
21citing papers in PubMed
2.5field-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

21 citing papers in PubMed, 31 citations in OpenAlex.

  1. LILRB4 Recruits SHP-1 to Enhance Oxidative Stress and Apoptosis, Aggravating Myocardial Ischemia-Reperfusion Injury.FASEB journal : official publication of the Federation of American Societies for Experimental Biology · 2026
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  13. An Update on the Multifaceted Roles of STAT3 in the Heart.Frontiers in cardiovascular medicine · 2019
    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

3 authors at 3 institutions in 1 country.

Fouad A ZoueinDepartment of Pharmacology and Toxicology; School of Medicine; and The Jackson Center for Heart Research at UMMC; The Cardiovascular-Renal Research Center; The University of Mississippi Medical Center; Jackson, MS USA.
Mazen Kurdi
George W Booz
Jackson College · USJackson Memorial Hospital · USUniversity 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 R01 HL088101
6 · The paper itself

Abstract

A substantial body of evidence has shown that signal transducer and activator of transcription 3 (STAT3) has an important role in the heart in protecting the myocardium from ischemia and oxidative stress. These actions are attributed to STAT3 functioning as a transcription factor in upregulating cardioprotective genes. Loss of STAT3 has been implicated as well in the pathogenesis of heart failure and, in that context and in addition to the loss of a cardioprotective gene program, nuclear STAT3 has been identified as a transcriptional repressor important for the normal functioning of the ubiquitin-proteasome system for protein degradation. The later finding establishes a genomic role for STAT3 in controlling cellular homeostasis in cardiac myocytes independent of stress. Surprisingly, although a well-studied area, very few downstream gene targets of STAT3 in the heart have been definitively identified. In addition, STAT3 is now known to induce gene expression by noncanonical means that are not well characterized in the heart. On the other hand, recent evidence has shown that STAT3 has important nongenomic actions in cardiac myocytes that affect microtubule stability, mitochondrial respiration, and autophagy. These extranuclear actions of STAT3 involve protein-protein interactions that are incompletely understood, as is their regulation in both the healthy and injured heart. Moreover, how the diverse genomic and nongenomic actions of STAT3 crosstalk with each other is unchartered territory. Here we present an overview of what is and is not known about both the genomic and nongenomic actions of STAT3 in the heart from a structure-function perspective that focuses on the impact of posttranslational modifications and oxidative stress in regulating the actions and interactions of STAT3. Even though we have learnt a great deal about the role played by STAT3 in the heart, much more awaits to be discovered.

Indexed as

autophagycardiac hypertrophycardiac remodelingheart failureJAKmicrotubule stabilityposttranslational modificationredoxSTAT3

Identifiers

PMID24069556
PMCPMC3772108
OpenAlexW1972503373

What OpenQuestion holds

Textmetadata
LicenceCC BY-NC
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.