ArticleSkeletal muscle2012
Metabolic remodeling agents show beneficial effects in the dystrophin-deficient mdx mouse model.
Article in Skeletal muscle, 2012. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 55 papers, 1 of them a synthesis that pooled it.
What it found
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The trial behind it
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Who cites it
55 citing papers in PubMed, 1 synthesis or guideline pooled it, 90 citations in OpenAlex.
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- Downstream Pathways of Dystrophin Deficiency in Duchenne Muscular Dystrophy: Implications for Muscle Degeneration and Regeneration.Journal of cachexia, sarcopenia and muscle · 2026Review
- Translational progress in the development of pharmacotherapies for Duchenne muscular dystrophy.Regenerative medicine · 2025Article
- Calpainopathy (limb-girdle muscular dystrophy type R1): clinical features, diagnostic approaches, and biotechnological treatment methods.Journal of neuromuscular diseases · 2025Review
- CD47-blocking antibody confers metabolic benefits against obesity.Cell reports. Medicine · 2025Article
- Mitochondria and Reactive Oxygen Species: The Therapeutic Balance of Powers for Duchenne Muscular Dystrophy.Cells · 2024Review
- Molecular pathways involved in the control of contractile and metabolic properties of skeletal muscle fibers as potential therapeutic targets for Duchenne muscular dystrophy.Frontiers in physiology · 2024Review
- Nuclear receptors as potential therapeutic targets in peripheral arterial disease and related myopathy.The FEBS journal · 2023Review
- Pharmacological inhibition of HDAC6 improves muscle phenotypes in dystrophin-deficient mice by downregulating TGF-β via Smad3 acetylation.Nature communications · 2022Article
- Effects of Low-Intensity and Long-Term Aerobic Exercise on the Psoas Muscle ofInternational journal of molecular sciences · 2022Article
- Skeletal Muscle Mitochondria Dysfunction in Genetic Neuromuscular Disorders with Cardiac Phenotype.International journal of molecular sciences · 2021Review
- Beneficial Role of Exercise in the Modulation ofAntioxidants (Basel, Switzerland) · 2021Review
- MetforminFrontiers in physiology · 2021Article
- Mitochondrial dysfunction and consequences in calpain-3-deficient muscle.Skeletal muscle · 2020Article
- Mitochondrial dysfunction in skeletal muscle of fukutin-deficient mice is resistant to exercise- and 5-aminoimidazole-4-carboxamide ribonucleotide-induced rescue.Experimental physiology · 2020Article
- Identification of therapeutics that target eEF1A2 and upregulate utrophin A translation in dystrophic muscles.Nature communications · 2020Article
- AMPK Complex Activation Promotes Sarcolemmal Repair in Dysferlinopathy.Molecular therapy : the journal of the American Society of Gene Therapy · 2020Article
- Mitochondrial Dysfunction Is an Early Consequence of Partial or Complete Dystrophin Loss inFrontiers in physiology · 2020Article
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
7 authors at 2 institutions in 1 country.
Funding
Abstract
backgroundDuchenne muscular dystrophy is a genetic disease involving a severe muscle wasting that is characterized by cycles of muscle degeneration/regeneration and culminates in early death in affected boys. Mitochondria are presumed to be involved in the regulation of myoblast proliferation/differentiation; enhancing mitochondrial activity with exercise mimetics (AMPK and PPAR-delta agonists) increases muscle function and inhibits muscle wasting in healthy mice. We therefore asked whether metabolic remodeling agents that increase mitochondrial activity would improve muscle function in mdx mice.
methodsTwelve-week-old mdx mice were treated with two different metabolic remodeling agents (GW501516 and AICAR), separately or in combination, for 4 weeks. Extensive systematic behavioral, functional, histological, biochemical, and molecular tests were conducted to assess the drug(s)' effects.
resultsWe found a gain in body and muscle weight in all treated mice. Histologic examination showed a decrease in muscle inflammation and in the number of fibers with central nuclei and an increase in fibers with peripheral nuclei, with significantly fewer activated satellite cells and regenerating fibers. Together with an inhibition of FoXO1 signaling, these results indicated that the treatments reduced ongoing muscle damage.
conclusionsThe three treatments produced significant improvements in disease phenotype, including an increase in overall behavioral activity and significant gains in forelimb and hind limb strength. Our findings suggest that triggering mitochondrial activity with exercise mimetics improves muscle function in dystrophin-deficient mdx mice.
Identifiers
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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.