ReviewJournal of cachexia, sarcopenia and muscle2026
Current Trends in Duchenne Muscular Dystrophy Research and Therapy: 3D Cardiac Modelling.
Review in Journal of cachexia, sarcopenia and muscle, 2026. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 3 papers.
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.
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.
Who cites it
3 citing papers in PubMed.
- Human cardiovascular organoids: Biomedical applications and ethical challenges.American heart journal plus : cardiology research and practice · 2026Review
- Review
- Current Trends in Duchenne Muscular Dystrophy Research and Therapy: 3D Cardiac Modelling.Journal of cachexia, sarcopenia and muscle · 2026Review
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
4 authors.
Funding
Abstract
Duchenne muscular dystrophy (DMD), caused by dystrophin deficiency, presents a multifaceted challenge that affects both skeletal muscle function and cardiomyocyte homeostasis, causing progressive degeneration and life-threatening cardiac complications by adolescence. Current treatments fail to prevent poor prognoses, and while FDA-approved therapies show promise in targeting dystrophin restoration, including RNA-based approaches and microdystrophin gene therapy, clinical evidence supporting their efficacy remains limited. Substantial challenges persist, particularly in achieving effective cardiac targeting, ensuring long-term safety and developing scalable treatments. Alternative therapies addressing muscle and cardiac pathophysiology are being explored alongside dystrophin-based approaches. DMD treatment is increasingly focusing on heart targeting with optimized cardiac-specific delivery strategies. Human-induced pluripotent stem cells (hiPSCs) enable DMD modelling, bridging pathophysiology and clinical phenotypes. DMD patient-specific hiPSC-derived cardiomyocytes (hiPSC-CMs) serve as in vitro models for disease mechanisms and therapy, with 3D cardiac models, either self-organizing (spheroids) or moulded, expanding on hiPSC-CMs to reflect cell interactions and myocardial tissue architecture. Advanced methods like 2D cell sheets, patches and engineered 3D human cardiac models show potential for improving cell engraftment and functional recovery in injured hearts, but their direct therapeutic application in DMD remains speculative due to extensive muscle mass loss; the complexity of cardiac and skeletal muscle interactions; and unresolved challenges related to cell integration, maturation and long-term function. Considering the premature state of cell-based therapies in this complex disease, current DMD treatment efforts focus on genetic approaches. Progress will likely depend on combining dystrophin-restoring strategies with therapies targeting disease mechanisms and improving cardiac delivery.
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Identifiers
What OpenQuestion holds
Registered trials
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.