ArticleFrontiers in physiology2021
Cardioprotective Effect of Whole Body Periodic Acceleration in Dystrophic Phenotype
Article in Frontiers in physiology, 2021. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 8 papers.
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Who cites it
8 citing papers in PubMed, 9 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
- Whole-body periodic acceleration: a new countermeasure against bone loss induced by long-term hindlimb unloading.European journal of applied physiology · 2026Article
- Cardioprotective effects of naringin in a type 2 diabetes rodent model by reducing calcium overload and oxidative stress.Frontiers in pharmacology · 2025Article
- Caveolin and NOS in the Development of Muscular Dystrophy.International journal of molecular sciences · 2024Review
- Right ventricular preload and afterload challenge induces contractile dysfunction and arrhythmia in isolated hearts of dystrophin-deficient male mice.Physiological reports · 2024Article
- Enhancing Muscle Intracellular CaBiomedicines · 2023Article
- Smooth Muscle Cells of Dystrophic (mdx) Mice Are More Susceptible to Hypoxia; The Protective Effect of Reducing CaBiomedicines · 2023Article
- The Role of the NaFrontiers in cellular and infection microbiology · 2022Article
Corrections and comments
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Authors and funding
5 authors at 4 institutions in 3 countries.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Duchenne muscular dystrophy (DMD) is characterized by progressive muscle wasting and the development of a dilated cardiomyopathy (DCM), which is the leading cause of death in DMD patients. Despite knowing the cause of DMD, there are currently no therapies which can prevent or reverse its inevitable progression. We have used whole body periodic acceleration (WBPA) as a novel tool to enhance intracellular constitutive nitric oxide (NO) production. WBPA adds small pulses to the circulation to increase pulsatile shear stress, thereby upregulating endothelial nitric oxide synthase (eNOS) and neuronal nitric oxide synthase (nNOS) and subsequently elevating the production of NO. Myocardial cells from dystrophin-deficient 15-month old
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Registered trials
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