Evidence map›Paper›PMID 40879110›Full record

ArticleFASEB journal : official publication of the Federation of American Societies for Experimental Biology2025

MYH6-Cre Insertion Accelerates Cardiac Phenotype in Dystrophic D2-mdx Mice.

India K Hawkins, Trung Phi, Joshua Mitchell, Frank Corwin, Adolfo G Mauro, Fadi N Salloum, Frank J Raucci

Abstract read
PubMed Full text at PMC Publisher
In one paragraph

Article in FASEB journal : official publication of the Federation of American Societies for Experimental Biology, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 1 paper.

0numbers the graph read from it
0cells of the map it votes in
1citing papers in PubMed
–field-weighted citation impact
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

1 citing paper in PubMed.

  1. MYH6-Cre Insertion Accelerates Cardiac Phenotype in Dystrophic D2-mdx Mice.FASEB journal : official publication of the Federation of American Societies for Experimental Biology · 2025
    Article
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.

India K HawkinsDivision of Pediatric Cardiology, Department of Pediatrics, Children's Hospital of Richmond at Virginia Commonwealth University, Richmond, Virginia, USA.
Trung PhiDivision of Pediatric Cardiology, Department of Pediatrics, Children's Hospital of Richmond at Virginia Commonwealth University, Richmond, Virginia, USA.
Joshua MitchellBioimaging and Applied Research Core, Virginia Commonwealth School of Medicine, Richmond, Virginia, USA.
Frank CorwinBioimaging and Applied Research Core, Virginia Commonwealth School of Medicine, Richmond, Virginia, USA.
Adolfo G MauroDivision of Pediatric Cardiology, Department of Pediatrics, Children's Hospital of Richmond at Virginia Commonwealth University, Richmond, Virginia, USA.
Fadi N SalloumPauley Heart Center, Division of Cardiology, Department of Internal Medicine, Virginia Commonwealth University School of Medicine, Richmond, Virginia, USA.
Frank J RaucciDivision of Pediatric Cardiology, Department of Pediatrics, Children's Hospital of Richmond at Virginia Commonwealth University, Richmond, Virginia, USA.

Funding

Virus Vector Shared ResourceP30CA016059 · NCI · VIRGINIA COMMONWEALTH UNIVERSITY · PI Renato Martins · 1985 to 2026
$51.0M
Managing Cardiac Toxicities of Cancer TherapyR35HL155651 · NHLBI · VIRGINIA COMMONWEALTH UNIVERSITY · PI Fadi N Salloum · 2021 to 2026
$4.6M
Targeting Pannexin 1 as a Novel Mechanism for Arrhythmia and Fibrosis in Duchenne CardiomyopathyK08HL155852 · NHLBI · VIRGINIA COMMONWEALTH UNIVERSITY · PI RAUCCI, FRANK J · 2021 to 2025
$742k
HHS | NIH | National Heart, Lung, and Blood Institute (NHLBI) K08HL155852HHS | NIH | National Heart, Lung, and Blood Institute (NHLBI) R35HL155651NCI NIH HHS P30 CA016059NHLBI NIH HHS K08 HL155852NHLBI NIH HHS R35 HL155651
6 · The paper itself

Abstract

Duchenne Muscular Dystrophy (DMD) is a progressive muscular degenerative disease that is recessively inherited through the X chromosome. Various mutations in the dystrophin gene lead to noticeable muscle weakness. The effects on skeletal and cardiac tissue result in progressive immobility and cardiac dysfunction, respectively. There are several murine models used to study DMD; however, there are still limitations in replicating the pathology of the disease seen in humans with DMD. Myh6cre(Cre) genotypic modification through the Cre/LoxP system has been proposed to further develop the pathology in murine models to specifically target cardiac tissue while allowing further alteration downstream in the mouse's lifespan. Initial observation of obesity in conjunction with premature death compared to traditional dystrophin-affected mice prompted us to take a further look into fibrosis and cardiac dysfunction. Our findings may help define the phenotype of dystrophin knockout, Cre-positive mice and display the potential for a more accurate, pathological model for DMD.

Indexed as

Cardiac MyosinsIntegrasesMuscular Dystrophy, DuchenneMyocardiumMyosin Heavy ChainsAnimalsDisease Models, AnimalDystrophinMaleMiceMice, Inbred mdxPhenotypeCardiac MyosinsCre recombinaseDystrophinIntegrasesMyh6 protein, mouseMyosin Heavy Chains

Identifiers

PMID40879110
PMCPMC12257423

What OpenQuestion holds

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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.