ReviewFrontiers in physiology2013
Functional muscle ischemia in Duchenne and Becker muscular dystrophy.
Review in Frontiers in physiology, 2013. The graph could read no effect estimate from its abstract, so it casts no vote on the map. It is linked to trial NCT06290713 (Vasodilators and Exercise as Adjuvant Therapy for Duchenne Muscular Dystrophy), which is not on this map. Cited by 47 papers, 1 of them a synthesis that pooled it.
What it found
Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.
The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
The trial behind it
Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.
Vasodilators and Exercise as Adjuvant Therapy for Duchenne Muscular Dystrophy (VASO-REx Study)
Who cites it
47 citing papers in PubMed, 1 synthesis or guideline pooled it, 83 citations in OpenAlex.
- Respiratory muscle training in children and adults with neuromuscular disease.The Cochrane database of systematic reviews · 2019Pooled it
- Article
- A Borophosphate Glass Doped with Cobalt Oxide Improves Skeletal Muscle Structure and Function in Myopathic Mice.Journal of functional biomaterials · 2026Article
- Unveiling the Potential of Bioactive Glass in Volumetric Muscle Loss Regeneration.Materials (Basel, Switzerland) · 2025Review
- A comprehensive spatiotemporal map of dystrophin isoform expression in the developing and adult human brain.Acta neuropathologica communications · 2025Article
- Enhanced expression of the myogenic factor Myocyte enhancer factor-2 in imaginal disc myoblasts activates a partial, but incomplete, muscle development program.Developmental biology · 2024Article
- Poor bone health in Duchenne muscular dystrophy: a multifactorial problem beyond corticosteroids and loss of ambulation.Frontiers in endocrinology · 2024Review
- Heart Disease in Mothers of Children with Duchenne Muscular Dystrophy.Current cardiology reviews · 2024Review
- Diversity and features of proteins with structural repeats.Biophysical reviews · 2023Review
- Microvascular Skeletal-Muscle Crosstalk in Health and Disease.International journal of molecular sciences · 2023Review
- iPSCs ameliorate hypoxia-induced autophagy and atrophy in C2C12 myotubes via the AMPK/ULK1 pathway.Biological research · 2023Article
- Vascular therapy for Duchenne muscular dystrophy (DMD).Faculty reviews · 2023Review
- Microvascular response to exercise varies along the length of the tibialis anterior muscle.NMR in biomedicine · 2022Article
- The Donnan-dominated resting state of skeletal muscle fibers contributes to resilience and longevity in dystrophic fibers.The Journal of general physiology · 2022Article
- Complexity of skeletal muscle degeneration: multi-systems pathophysiology and organ crosstalk in dystrophinopathy.Pflugers Archiv : European journal of physiology · 2021Review
- A split-label design for simultaneous measurements of perfusion in distant slices by pulsed arterial spin labeling.Magnetic resonance in medicine · 2021Article
- Dystrophin deficiency impairs vascular structure and function in the canine model of Duchenne muscular dystrophy.The Journal of pathology · 2021Article
- Hypoxia and Hypoxia-Inducible Factor Signaling in Muscular Dystrophies: Cause and Consequences.International journal of molecular sciences · 2021Review
- VEGFR-1/Flt-1 inhibition increases angiogenesis and improves muscle function in a mouse model of Duchenne muscular dystrophy.Molecular therapy. Methods & clinical development · 2021Article
- Therapeutic aspects of cell signaling and communication in Duchenne muscular dystrophy.Cellular and molecular life sciences : CMLS · 2021Review
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
1 author at 1 institution in 1 country.
Funding
Abstract
Duchenne and Becker muscular dystrophy (DMD/BMD) comprise a spectrum of devastating X-linked muscle wasting disease for which there is no treatment. DMD/BMD is caused by mutations in the gene encoding dystrophin, a cytoskeletal protein that stabilizes the muscle membrane and also targets other proteins to the sarcolemma. Among these is the muscle-specific isoform of neuronal nitric oxide synthase (nNOSμ) which binds spectrin-like repeats within dystrophin's rod domain and the adaptor protein α-syntrophin. Dystrophin deficiency causes loss of sarcolemmal nNOSμ and reduces paracrine signaling of muscle-derived nitric oxide (NO) to the microvasculature, which renders the diseased muscle fibers susceptible to functional muscle ischemia during exercise. Repeated bouts of functional ischemia superimposed on muscle fibers already weakened by dystrophin deficiency result in use-dependent focal muscle injury. Genetic and pharmacologic strategies to boost nNOSμ-NO signaling in dystrophic muscle alleviate functional muscle ischemia and show promise as novel therapeutic interventions for the treatment of DMD/BMD.
Indexed as
Identifiers
What OpenQuestion holds
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.