Evidence map›Paper›PMID 35818510›Full record

ReviewJACC. Basic to translational science2022

Cardiovascular Disease in Duchenne Muscular Dystrophy: Overview and Insight Into Novel Therapeutic Targets.

Taylor I Schultz, Frank J Raucci, Fadi N Salloum

Open access · goldAbstract readReview
In one paragraph

Review in JACC. Basic to translational science, 2022. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 52 papers.

0numbers the graph read from it
0cells of the map it votes in
52citing papers in PubMed
4.4field-weighted citation impact, top 4% 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

52 citing papers in PubMed, 56 citations in OpenAlex.

  1. Trial
  2. Article
  3. Article
  4. CRISPR-Cas9-mediated upregulation of utrophin ameliorates Duchenne muscular dystrophy.Molecular therapy : the journal of the American Society of Gene Therapy · 2026
    Article
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  11. Review
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  18. Cardiac fibrosis: from mechanisms and models to medicines.Trends in pharmacological sciences · 2025
    Review
  19. Review
  20. 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

3 authors at 1 institution in 1 country.

Taylor I SchultzDepartment of Physiology and Biophysics, Virginia Commonwealth University, Richmond, Virginia, USA.
Frank J RaucciDepartment of Physiology and Biophysics, Virginia Commonwealth University, Richmond, Virginia, USA.
Fadi N SalloumDepartment of Physiology and Biophysics, Virginia Commonwealth University, Richmond, Virginia, USA.
Virginia Commonwealth University · US

Funding

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
NHLBI NIH HHS K08 HL155852
6 · The paper itself

Abstract

Duchenne muscular dystrophy (DMD) is a devastating disease affecting approximately 1 in every 3,500 male births worldwide. Multiple mutations in the dystrophin gene have been implicated as underlying causes of DMD. However, there remains no cure for patients with DMD, and cardiomyopathy has become the most common cause of death in the affected population. Extensive research is under way investigating molecular mechanisms that highlight potential therapeutic targets for the development of pharmacotherapy for DMD cardiomyopathy. In this paper, the authors perform a literature review reporting on recent ongoing efforts to identify novel therapeutic strategies to reduce, prevent, or reverse progression of cardiac dysfunction in DMD.

Indexed as

ACE, angiotensin-converting enzymeApN, adiponectinARB, angiotensin receptor blockerarrhythmiasBB, beta-blockerBDNF, brain-derived neurotrophic factorcardiomyopathyCMR, cardiac magnetic resonance imagingCx, connexinDMD, Duchenne muscular dystrophyDPC, dystrophin-associated protein complexDuchenne muscular dystrophyFFA, free fatty acidHF, heart failureinflammatory modulatorsLNP, lipid nanoparticleLVEF, left ventricular ejection fractionLV, left ventricularmiR, microRNAmyocardial fibrosisNIV, noninvasive ventilationNrf2, nuclear factor erythroid 2-related factor 2PKA, protein kinase APTX3, pentraxin 3Px, pannexinRNP, ribonucleoprotein complexesRT-qPCR, reverse transcription-quantitative polymerase chain reactionRyR2, ryanodine receptor isoform 2sgRNA, single guide RNASR, sarcoplasmic reticulumTrkB, tyrosine kinase BTRPV2, transient receptor potential cation channel, subfamily V, member 2

Identifiers

PMID35818510
PMCPMC9270569
OpenAlexW4220711760

What Socratic 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 Socratic graph.