ArticleJournal of cachexia, sarcopenia and muscle2019
Early myopathy in Duchenne muscular dystrophy is associated with elevated mitochondrial H
Article in Journal of cachexia, sarcopenia and muscle, 2019. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 76 papers.
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Who cites it
76 citing papers in PubMed, 131 citations in OpenAlex.
- Serum biomarkers associated with baseline clinical severity in young steroid-naïve Duchenne muscular dystrophy boys.Human molecular genetics · 2020Trial
- Basal Energetics and Phosphocreatine Recovery Kinetics in Ambulatory Boys With Duchenne Muscular Dystrophy.NMR in biomedicine · 2026Article
- Acute mitochondrial dysfunction impairs neuromuscular transmission and contractility in mouse diaphragm: the protective potential of 25-hydroxycholesterol.Journal of physiology and biochemistry · 2026Article
- BCL6 regulates skeletal muscle mass and mitochondrial bioenergetics.Molecular metabolism · 2026Article
- Targeting autophagy in Duchenne muscular dystrophy: mechanistic insights and emerging therapeutic strategies.Journal of medical genetics · 2026Review
- The D2.B10-DmdThe American journal of pathology · 2026Article
- Parkin overexpression attenuates muscle atrophy and improves mitochondrial bioenergetics but not histological features of Duchenne muscular dystrophy in mice.Scientific reports · 2026Article
- Volitional exercise elicits physiological and molecular improvements in the severe D2.mdx mouse model of Duchenne muscular dystrophy.The Journal of physiology · 2026Article
- The miR-30c-5p/SOCS3 axis is a potential driver of inflammation and metabolic imbalance in Duchenne muscular dystrophy.Frontiers in cell and developmental biology · 2026Article
- Histone deacetylases in Duchenne muscular dystrophy: a role in the mechanism of disease and a target for inhibition.Clinical epigenetics · 2025Review
- Early Taurine Administration Decreases the Levels of Receptor-Interacting Serine/Threonine Protein Kinase 1 in the Duchenne Mouse ModelBrain sciences · 2025Article
- Mitochondrial-targeted plastoquinone therapy prevents early onset muscle weakness that occurs before atrophy during ovarian cancer.Molecular metabolism · 2025Article
- Inhibition of mitochondrial fission protein Drp1 ameliorates skeletal myopathy in the D2-mdx model of Duchenne muscular dystrophy.American journal of physiology. Cell physiology · 2025Article
- Understanding Duchenne muscular dystrophy-associated brain pathology.Disease models & mechanisms · 2025Review
- Delivery of A Chemically Modified Noncoding RNA Domain Improves Dystrophic Myotube Function.Advanced science (Weinheim, Baden-Wurttemberg, Germany) · 2025Article
- Evaluation of the redox alteration in Duchenne muscular dystrophy model mice using in vivo DNP-MRI.Npj imaging · 2024Article
- Measurement of Mitochondrial Respiration in Human and Mouse Skeletal Muscle Fibers by High-Resolution Respirometry.Journal of visualized experiments : JoVE · 2024Article
- Cardiac Atrophy, Dysfunction, and Metabolic Impairments: A Cancer-Induced Cardiomyopathy Phenotype.The American journal of pathology · 2024Article
- Respiratory performance in Duchenne muscular dystrophy: Clinical manifestations and lessons from animal models.Experimental physiology · 2024Review
- Muscle weakness and mitochondrial stress occur before severe metastasis in a novel mouse model of ovarian cancer cachexia.Molecular metabolism · 2024Article
16 more citing papers are in PubMed but not listed here.
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Authors and funding
15 authors at 4 institutions in 2 countries.
Funding
No grant is acknowledged in the PubMed record.
Abstract
backgroundMuscle wasting and weakness in Duchenne muscular dystrophy (DMD) causes severe locomotor limitations and early death due in part to respiratory muscle failure. Given that current clinical practice focuses on treating secondary complications in this genetic disease, there is a clear need to identify additional contributions in the aetiology of this myopathy for knowledge-guided therapy development. Here, we address the unresolved question of whether the complex impairments observed in DMD are linked to elevated mitochondrial H
methodsMitochondrial bioenergetics were compared with functional and histopathological indices of myopathy early in DMD (4 weeks) in D2.B10-DMD
resultsPathway-specific analyses revealed that Complex I-supported maximal H
conclusionsThese results provide evidence that Complex I dysfunction and loss of central respiratory control by ADP and creatine cause elevated oxidant generation during impaired oxidative phosphorylation. These dysfunctions may contribute to early stage disease pathophysiology and support the growing notion that mitochondria are a potential therapeutic target in this disease.
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