ArticleSkeletal muscle2020
Mechanical factors tune the sensitivity of mdx muscle to eccentric strength loss and its protection by antioxidant and calcium modulators.
Article in Skeletal muscle, 2020. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 25 papers.
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25 citing papers in PubMed, 43 citations in OpenAlex.
- Cytoplasmic region of beta-dystroglycan is essential for postsynaptic maturation and neuromuscular function in mice.Proceedings of the National Academy of Sciences of the United States of America · 2026Article
- Viscoelastic properties of dystrophin-deficient mouse skeletal muscles are resilient to isometric fatiguing exercise.Physiological reports · 2026Article
- Twisting Paths: The Paradox of Fiber Branching in Muscle Regeneration.International journal of molecular sciences · 2026Review
- Dysferlin and the Regulation of CaCells · 2025Review
- Myo-MOVES: a custom electrical stimulation system for functional studies of 3D bioengineered muscle.Lab on a chip · 2025Article
- Dysregulated ATX-LPA and YAP/TAZ signaling in dystrophic SgcdSkeletal muscle · 2025Article
- Longitudinal trajectories of muscle impairments in growing boys with Duchenne muscular dystrophy.PloS one · 2025Article
- Article
- Exploring lipin1 as a promising therapeutic target for the treatment of Duchenne muscular dystrophy.Journal of translational medicine · 2024Article
- Time-of-day effects on ex vivo muscle contractility following short-term satellite cell ablation.American journal of physiology. Cell physiology · 2024Article
- Modulating fast skeletal muscle contraction protects skeletal muscle in animal models of Duchenne muscular dystrophy.The Journal of clinical investigation · 2023Article
- Eccentric contraction-induced strength loss in dystrophin-deficient muscle: Preparations, protocols, and mechanisms.The Journal of general physiology · 2023Article
- Six weeks of N-acetylcysteine antioxidant in drinking water decreases pathological fiber branching in MDX mouse dystrophic fast-twitch skeletal muscle.Frontiers in physiology · 2023Article
- RYR-1-Related Diseases International Research Workshop: From Mechanisms to Treatments Pittsburgh, PA, U.S.A., 21-22 July 2022.Journal of neuromuscular diseases · 2023Article
- Postdevelopmental knockout of Orai1 improves muscle pathology in a mouse model of Duchenne muscular dystrophy.The Journal of general physiology · 2022Article
- Mechanisms of weakness in Mdx muscle following in vivo eccentric contractions.Journal of muscle research and cell motility · 2022Article
- Loss of α-actinin-3 confers protection from eccentric contraction damage in fast-twitch EDL muscles from aged mdx dystrophic mice by reducing pathological fibre branching.Human molecular genetics · 2022Article
- Longitudinal Alterations in Gait Features in Growing Children With Duchenne Muscular Dystrophy.Frontiers in human neuroscience · 2022Article
- The beneficial effect of chronic muscular exercise on muscle fragility is increased by Prox1 gene transfer in dystrophic mdx muscle.PloS one · 2022Article
- Pharmacological activation of SERCA ameliorates dystrophic phenotypes in dystrophin-deficient mdx mice.Human molecular genetics · 2021Article
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Authors and funding
10 authors at 1 institution in 2 countries.
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Abstract
backgroundDystrophin deficiency sensitizes skeletal muscle of mice to eccentric contraction (ECC)-induced strength loss. ECC protocols distinguish dystrophin-deficient from healthy, wild type muscle, and test the efficacy of therapeutics for Duchenne muscular dystrophy (DMD). However, given the large lab-to-lab variability in ECC-induced strength loss of dystrophin-deficient mouse skeletal muscle (10-95%), mechanical factors of the contraction likely impact the degree of loss. Therefore, the purpose of this study was to evaluate the extent to which mechanical variables impact sensitivity of dystrophin-deficient mouse skeletal muscle to ECC.
methodsWe completed ex vivo and in vivo muscle preparations of the dystrophin-deficient mdx mouse and designed ECC protocols within physiological ranges of contractile parameters (length change, velocity, contraction duration, and stimulation frequencies). To determine whether these contractile parameters affected known factors associated with ECC-induced strength loss, we measured sarcolemmal damage after ECC as well as strength loss in the presence of the antioxidant N-acetylcysteine (NAC) and small molecule calcium modulators that increase SERCA activity (DS-11966966 and CDN1163) or lower calcium leak from the ryanodine receptor (Chloroxine and Myricetin).
resultsThe magnitude of length change, work, and stimulation duration ex vivo and in vivo of an ECC were the most important determinants of strength loss in mdx muscle. Passive lengthening and submaximal stimulations did not induce strength loss. We further showed that sarcolemmal permeability was associated with muscle length change, but it only accounted for a minimal fraction (21%) of the total strength loss (70%). The magnitude of length change also significantly influenced the degree to which NAC and small molecule calcium modulators protected against ECC-induced strength loss.
conclusionsThese results indicate that ECC-induced strength loss of mdx skeletal muscle is dependent on the mechanical properties of the contraction and that mdx muscle is insensitive to ECC at submaximal stimulation frequencies. Rigorous design of ECC protocols is critical for effective use of strength loss as a readout in evaluating potential therapeutics for muscular dystrophy.
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