Evidence map›Paper›PMID 23364341›Full record

ArticleHypertension research : official journal of the Japanese Society of Hypertension2013

Role of STAT3 in angiotensin II-induced hypertension and cardiac remodeling revealed by mice lacking STAT3 serine 727 phosphorylation.

Fouad A Zouein, Carlos Zgheib, Shereen Hamza, John W Fuseler, John E Hall, Andrea Soljancic, Arnaldo Lopez-Ruiz, Mazen Kurdi, George W Booz

Open access · bronzeAbstract read
In one paragraph

Article in Hypertension research : official journal of the Japanese Society of Hypertension, 2013. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 24 papers.

0numbers the graph read from it
0cells of the map it votes in
24citing papers in PubMed
1.3field-weighted citation impact, top 20% 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

24 citing papers in PubMed, 45 citations in OpenAlex.

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  7. GRK5 is a regulator of fibroblast activation and cardiac fibrosis.Proceedings of the National Academy of Sciences of the United States of America · 2021
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  13. The nuclear receptor RORα protects against angiotensin II-induced cardiac hypertrophy and heart failure.American journal of physiology. Heart and circulatory physiology · 2019
    Article
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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

9 authors at 4 institutions in 2 countries.

Fouad A ZoueinDepartment of Pharmacology and Toxicology, and Center for Excellence in Cardiovascular-Renal Research, The University of Mississippi Medical Center, School of Medicine, Jackson, MS, USA.
Carlos Zgheib
Shereen Hamza
John W Fuseler
John E Hall
Andrea Soljancic
Arnaldo Lopez-Ruiz
Mazen Kurdi
George W Booz
University of Mississippi Medical Center · USJackson Memorial Hospital · USRafik Hariri University · LBUniversity of South Carolina · 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 5R01HL088101-06NHLBI NIH HHS R01 HL088101
6 · The paper itself

Abstract

STAT3 is involved in protection of the heart provided by ischemic preconditioning. However, the role of this transcription factor in the heart in chronic stresses such as hypertension has not been defined. We assessed whether STAT3 is important in hypertension-induced cardiac remodeling using mice with reduced STAT3 activity due to a S727A mutation (SA/SA). Wild type (WT) and SA/SA mice received angiotensin (ANG) II or saline for 17 days. ANG II increased mean arterial and systolic pressure in SA/SA and WT mice, but cardiac levels of cytokines associated with heart failure were increased less in SA/SA mice. Unlike WT mice, hearts of SA/SA mice showed signs of developing systolic dysfunction as evidenced by reduction in ejection fraction and fractional shortening. In the left ventricle of both WT and SA/SA mice, ANG II induced fibrosis. However, fibrosis in SA/SA mice appeared more extensive and was associated with loss of myocytes. Cardiac hypertrophy as indexed by heart to body weight ratio and left ventricular anterior wall dimension during diastole was greater in WT mice. In WT+ANG II mice there was an increase in the mass of individual myofibrils. In contrast, cardiac myocytes of SA/SA+ANG II mice showed a loss in myofibrils and myofibrillar mass density was decreased during ANG II infusion. Our findings reveal that STAT3 transcriptional activity is important for normal cardiac myocyte myofibril morphology. Loss of STAT3 may impair cardiac function in the hypertensive heart due to defective myofibrillar structure and remodeling that may lead to heart failure.

Indexed as

Angiotensin IIIschemic Preconditioning, MyocardialVasoconstrictor AgentsAnimalsBlood PressureCardiomegalyCollagenCytokinesElectrocardiographyFibrosisHeartHemodynamicsHypertensionMiceMice, Inbred C57BLMice, TransgenicAngiotensin IICollagenCytokinesSerineStat3 protein, mouseSTAT3 Transcription FactorVasoconstrictor Agents

Identifiers

PMID23364341
PMCPMC3674130
OpenAlexW2029567799

What OpenQuestion holds

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Read underepoch 390

Registered trials

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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.