ArticlePloS one2015
Metabolic dysfunction and altered mitochondrial dynamics in the utrophin-dystrophin deficient mouse model of duchenne muscular dystrophy.
Article in PloS one, 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 51 papers.
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Who cites it
51 citing papers in PubMed, 66 citations in OpenAlex.
- Prolonged sepsis triggers abnormal mitochondrial dynamics in the limb muscles and diaphragm.Molecular and cellular biochemistry · 2025Article
- A consensus guide to preclinical indirect calorimetry experiments.Nature metabolism · 2025Review
- The human genetic variant rs6190 unveils Foxc1 and Arid5a as novel prometabolic targets of the glucocorticoid receptor in muscle.Science advances · 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
- Reduced voltage-activated Ca2+ release flux in muscle fibers from a rat model of Duchenne dystrophy.The Journal of general physiology · 2025Article
- An Orai1 gain-of-function tubular aggregate myopathy mouse model phenocopies key features of the human disease.The EMBO journal · 2024Article
- Autophagy in Muscle Regeneration: Mechanisms, Targets, and Therapeutic Perspective.International journal of molecular sciences · 2024Review
- Improved mitochondrial function in the hearts of sarcolipin-deficient dystrophin and utrophin double-knockout mice.JCI insight · 2024Article
- Mitochondria and Reactive Oxygen Species: The Therapeutic Balance of Powers for Duchenne Muscular Dystrophy.Cells · 2024Review
- Mitochondrial Transplantation Therapy Ameliorates Muscular Dystrophy inBiomolecules · 2024Article
- Cellular pathogenesis of Duchenne muscular dystrophy: progressive myofibre degeneration, chronic inflammation, reactive myofibrosis and satellite cell dysfunction.European journal of translational myology · 2023Article
- Article
- Ion Channels of the Sarcolemma and Intracellular Organelles in Duchenne Muscular Dystrophy: A Role in the Dysregulation of Ion Homeostasis and a Possible Target for Therapy.International journal of molecular sciences · 2023Review
- Duchenne muscular dystrophy: disease mechanism and therapeutic strategies.Frontiers in physiology · 2023Review
- Satellite cell contribution to disease pathology in Duchenne muscular dystrophy.Frontiers in physiology · 2023Review
- Chlamydia trachomatis Alters Mitochondrial Protein Composition and Secretes Effector Proteins That Target Mitochondria.mSphere · 2022Article
- Histological Methods to Assess Skeletal Muscle Degeneration and Regeneration in Duchenne Muscular Dystrophy.International journal of molecular sciences · 2022Review
- BKPharmaceutics · 2022Article
- Mitochondrial Dysfunction as an Underlying Cause of Skeletal Muscle Disorders.International journal of molecular sciences · 2022Review
- Article
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Authors and funding
7 authors at 1 institution in 1 country.
Funding
Abstract
The utrophin-dystrophin deficient (DKO) mouse model has been widely used to understand the progression of Duchenne muscular dystrophy (DMD). However, it is unclear as to what extent muscle pathology affects metabolism. Therefore, the present study was focused on understanding energy expenditure in the whole animal and in isolated extensor digitorum longus (EDL) muscle and to determine changes in metabolic enzymes. Our results show that the 8 week-old DKO mice consume higher oxygen relative to activity levels. Interestingly the EDL muscle from DKO mouse consumes higher oxygen per unit integral force, generates less force and performs better in the presence of pyruvate thus mimicking a slow twitch muscle. We also found that the expression of hexokinase 1 and pyruvate kinase M2 was upregulated several fold suggesting increased glycolytic flux. Additionally, there is a dramatic increase in dynamin-related protein 1 (Drp 1) and mitofusin 2 protein levels suggesting increased mitochondrial fission and fusion, a feature associated with increased energy demand and altered mitochondrial dynamics. Collectively our studies point out that the dystrophic disease has caused significant changes in muscle metabolism. To meet the increased energetic demand, upregulation of metabolic enzymes and regulators of mitochondrial fusion and fission is observed in the dystrophic muscle. A better understanding of the metabolic demands and the accompanied alterations in the dystrophic muscle can help us design improved intervention therapies along with existing drug treatments for the DMD patients.
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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.