ArticleThe Journal of clinical investigation2023
Modulating fast skeletal muscle contraction protects skeletal muscle in animal models of Duchenne muscular dystrophy.
Article in The Journal of clinical investigation, 2023. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 25 papers.
What it found
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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.
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Who cites it
25 citing papers in PubMed, 32 citations in OpenAlex.
- Trial
- Testosterone Modulation of Muscle Transcriptomic Profile During Lifestyle Therapy in Older Men with Obesity and Hypogonadism.Journal of cachexia, sarcopenia and muscle · 2025Trial
- Downstream Pathways of Dystrophin Deficiency in Duchenne Muscular Dystrophy: Implications for Muscle Degeneration and Regeneration.Journal of cachexia, sarcopenia and muscle · 2026Review
- Systemic regeneration medicines for muscular dystrophy: progress and challenges in pro-regenerative drug development.Cell regeneration (London, England) · 2026Review
- Effects of sevasemten (EDG-5506) on safety, biomarkers, and functional measures in adults with Becker muscular dystrophy: results of a phase 1b, open-label study.EBioMedicine · 2026Article
- Human Disposition, Metabolism, and Excretion of Sevasemten (EDG-5506), a Selective Modulator of Fast Myosin in Healthy Volunteers.Journal of clinical pharmacology · 2026Article
- Open-Source Tools for Neuromuscular Electrical Stimulation in Mouse Models: A Methodological Validation Study.Muscles (Basel, Switzerland) · 2026Article
- Duchenne Muscular Dystrophy: Contemporary Therapeutic Options and Real-World Challenges in Treatment Selection.Muscles (Basel, Switzerland) · 2026Review
- Functional and structural pathologies in skeletal muscle of a rat model of Duchenne muscular dystrophy.Skeletal muscle · 2026Article
- Twisting Paths: The Paradox of Fiber Branching in Muscle Regeneration.International journal of molecular sciences · 2026Review
- Fast Myosin Binding Protein-C Is a Vital Regulator in Young and Aged Fast Skeletal Muscle Homeostasis.Journal of cachexia, sarcopenia and muscle · 2025Article
- Bidirectional role of Costameres in the pathophysiology of mdx skeletal muscles.Human molecular genetics · 2025Article
- Translational progress in the development of pharmacotherapies for Duchenne muscular dystrophy.Regenerative medicine · 2025Article
- Short-term daily deflazacort decreases membrane permeability and increases maximum force inAmerican journal of physiology. Cell physiology · 2025Article
- Transcriptome Analysis of Muscle Tissue from Three Anatomical Locations in Male and Female Kazakh Horses.Biology · 2025Article
- Transcriptomic profiling of skeletal muscle in the DMDScientific reports · 2025Article
- Longitudinal Changes of Motor Function in Becker Muscular Dystrophy.Neurology. Genetics · 2025Article
- Fatigue Resistance and Mitochondrial Adaptations to Isometric Interval Training in Dystrophin-Deficient Muscle: Role of Contractile Load.FASEB journal : official publication of the Federation of American Societies for Experimental Biology · 2025Article
- Beta-hydroxy-beta-methylbutyrate (HMB) improves daily activity and whole-body protein metabolism in Duchenne muscular dystrophy dogs: a pilot study.Scientific reports · 2025Article
- Clinical Characteristics of Patients With Becker Muscular Dystrophy Having Pathogenic Microvariants or Duplications.Neurology. Genetics · 2025Article
Corrections and comments
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Authors and funding
28 authors at 7 institutions in 2 countries.
Funding
Abstract
Duchenne muscular dystrophy (DMD) is a lethal muscle disease caused by absence of the protein dystrophin, which acts as a structural link between the basal lamina and contractile machinery to stabilize muscle membranes in response to mechanical stress. In DMD, mechanical stress leads to exaggerated membrane injury and fiber breakdown, with fast fibers being the most susceptible to damage. A major contributor to this injury is muscle contraction, controlled by the motor protein myosin. However, how muscle contraction and fast muscle fiber damage contribute to the pathophysiology of DMD has not been well characterized. We explored the role of fast skeletal muscle contraction in DMD with a potentially novel, selective, orally active inhibitor of fast skeletal muscle myosin, EDG-5506. Surprisingly, even modest decreases of contraction (<15%) were sufficient to protect skeletal muscles in dystrophic mdx mice from stress injury. Longer-term treatment also decreased muscle fibrosis in key disease-implicated tissues. Importantly, therapeutic levels of myosin inhibition with EDG-5506 did not detrimentally affect strength or coordination. Finally, in dystrophic dogs, EDG-5506 reversibly reduced circulating muscle injury biomarkers and increased habitual activity. This unexpected biology may represent an important alternative treatment strategy for Duchenne and related myopathies.
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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.