Evidence map›Paper›PMID 40922015›Full record

ReviewSkeletal muscle2025

Fighting for every beat: cardiac therapies in Duchenne muscular dystrophy.

Antoine Muchir

Abstract readReview
In one paragraph

Review in Skeletal muscle, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 5 papers.

0numbers the graph read from it
0cells of the map it votes in
5citing 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

5 citing papers in PubMed.

  1. Article
  2. Article
  3. Article
  4. Article
  5. 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

1 author.

Antoine MuchirSorbonne Université, Inserm, Institut de Myologie, Centre de Recherche en Myologie, Paris, France. antoine.muchir@inserm.fr.

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Duchenne muscular dystrophy (DMD) is a severe, progressive genetic disorder caused by mutations in the DMD gene, resulting in the absence of dystrophin-a key structural protein at the sarcolemma. As the disease progresses, cardiac involvement becomes a leading cause of morbidity and mortality. By adolescence or early adulthood, many patients develop dilated cardiomyopathy and arrhythmias. Like skeletal muscle, cardiac muscle in DMD patients lacks dystrophin and undergoes similar degenerative changes, ultimately leading to ventricular dilation, systolic dysfunction, and heart failure. Early detection and proactive management of cardiac dysfunction are essential for optimizing outcomes. Despite significant advances and decades of research, a definitive cure for DMD remains elusive. In recognition of World Duchenne Awareness Day, this review highlights current and emerging therapeutic strategies with the potential to transform cardiac care in DMD and improve the lives of those affected.

Indexed as

Arrhythmias, CardiacCardiomyopathy, DilatedMuscular Dystrophy, DuchenneDystrophinHumansDystrophinDuchenne muscular dystrophyHeartInflammationMicro-dystrophinTherapies

Identifiers

PMID40922015
PMCPMC12418671

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.