ArticlePloS one2014
Whole body periodic acceleration is an effective therapy to ameliorate muscular dystrophy in mdx mice.
Article in PloS one, 2014. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 20 papers.
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Who cites it
20 citing papers in PubMed, 25 citations in OpenAlex.
- A Nonrandomized Trial of the Effects of Passive Simulated Jogging on Short-Term Heart Rate Variability in Type 2 Diabetic Subjects.Journal of diabetes research · 2023Trial
- The Effects of Passive Simulated Jogging on Parameters of Explosive Handgrip in Nondiabetics and Type 2 Diabetics: A Single Arm Study.BioMed research international · 2022Trial
- Whole-body periodic acceleration: a new countermeasure against bone loss induced by long-term hindlimb unloading.European journal of applied physiology · 2026Article
- DjCapon Affects the Neural Regeneration and Light Sensitivity via NO and Wnt5a Signaling in Planarian Dugesia japonica.Molecular neurobiology · 2025Article
- The Physiological Function of nNOS-Associated CAPON Proteins and the Roles of CAPON in Diseases.International journal of molecular sciences · 2023Review
- Smooth Muscle Cells of Dystrophic (mdx) Mice Are More Susceptible to Hypoxia; The Protective Effect of Reducing CaBiomedicines · 2023Article
- The Donnan-dominated resting state of skeletal muscle fibers contributes to resilience and longevity in dystrophic fibers.The Journal of general physiology · 2022Article
- Chronic Elevation of Skeletal Muscle [CaFrontiers in physiology · 2022Article
- Molecular Modification of Transient Receptor Potential Canonical 6 Channels Modulates Calcium Dyshomeostasis in a Mouse Model Relevant to Malignant Hyperthermia.Anesthesiology · 2021Article
- Physiological and Pathological Relevance of Selective and Nonselective CaAdvances in experimental medicine and biology · 2021Article
- Cardioprotective Effect of Whole Body Periodic Acceleration in Dystrophic PhenotypeFrontiers in physiology · 2021Article
- Contribution of TRPC Channels to Intracellular CaFrontiers in physiology · 2020Article
- Senescence Is Associated With Elevated Intracellular Resting [CaFrontiers in physiology · 2020Article
- Targeting angiogenesis in Duchenne muscular dystrophy.Cellular and molecular life sciences : CMLS · 2019Review
- DP71 and SERCA2 alteration in human neurons of a Duchenne muscular dystrophy patient.Stem cell research & therapy · 2019Article
- Enhancing Endogenous Nitric Oxide by Whole Body Periodic Acceleration Elicits Neuroprotective Effects in Dystrophic Neurons.Molecular neurobiology · 2018Article
- Adeno-associated virus serotype 9 mediated vascular endothelial growth factor gene overexpression in mdx mice.Experimental and therapeutic medicine · 2018Article
- Dysregulation of Intracellular CaMolecular neurobiology · 2018Article
- Assessment of muscle function using hybrid PET/MRI: comparison ofEuropean journal of nuclear medicine and molecular imaging · 2017Article
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Corrections and comments
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Authors and funding
8 authors at 6 institutions in 1 country.
Funding
Abstract
Duchenne muscular dystrophy (DMD) is a genetic disorder caused by the absence of dystrophin in both skeletal and cardiac muscles. This leads to severe muscle degeneration, and dilated cardiomyopathy that produces patient death, which in most cases occurs before the end of the second decade. Several lines of evidence have shown that modulators of nitric oxide (NO) pathway can improve skeletal muscle and cardiac function in the mdx mouse, a mouse model for DMD. Whole body periodic acceleration (pGz) is produced by applying sinusoidal motion to supine humans and in standing conscious rodents in a headward-footward direction using a motion platform. It adds small pulses as a function of movement frequency to the circulation thereby increasing pulsatile shear stress to the vascular endothelium, which in turn increases production of NO. In this study, we examined the potential therapeutic properties of pGz for the treatment of skeletal muscle pathology observed in the mdx mouse. We found that pGz (480 cpm, 8 days, 1 hr per day) decreased intracellular Ca(2+) and Na(+) overload, diminished serum levels of creatine kinase (CK) and reduced intracellular accumulation of Evans Blue. Furthermore, pGz increased muscle force generation and expression of both utrophin and the carboxy-terminal PDZ ligand of nNOS (CAPON). Likewise, pGz (120 cpm, 12 h) applied in vitro to skeletal muscle myotubes reduced Ca(2+) and Na(+) overload, diminished abnormal sarcolemmal Ca(2+) entry and increased phosphorylation of endothelial NOS. Overall, this study provides new insights into the potential therapeutic efficacy of pGz as a non-invasive and non-pharmacological approach for the treatment of DMD patients through activation of the NO pathway.
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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.