ArticleArteriosclerosis, thrombosis, and vascular biology2004
Absence of dystrophin in mice reduces NO-dependent vascular function and vascular density: total recovery after a treatment with the aminoglycoside gentamicin.
Article in Arteriosclerosis, thrombosis, and vascular biology, 2004. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 53 papers, 1 of them a synthesis that pooled it.
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Who cites it
53 citing papers in PubMed, 1 synthesis or guideline pooled it, 96 citations in OpenAlex.
- Muscle and cardiac therapeutic strategies for Duchenne muscular dystrophy: past, present, and future.Pharmacological reports : PR · 2020Pooled it
- Bilateral perifoveal macular ischemia in non-proliferative Duchenne muscular dystrophy-associated retinopathy: a case report.Documenta ophthalmologica. Advances in ophthalmology · 2026Article
- Genetic strategies for therapy of Duchenne muscular dystrophy.Molecular therapy. Nucleic acids · 2025Review
- Multiphoton microscopy and tissue clearing for 3D characterization of the vasculature and fibrosis remodeling in rat dystrophic skeletal muscle.Scientific reports · 2025Article
- Cell therapy for Duchenne muscular dystrophy: promises, challenges, and controversies.Cellular and molecular life sciences : CMLS · 2025Review
- Lymphatic dysfunction is linked to disease pathogenesis in Duchenne muscular dystrophy animal models.Proceedings of the National Academy of Sciences of the United States of America · 2025Article
- Exploring lncRNA-Mediated Mechanisms in Muscle Regulation and Their Implications for Duchenne Muscular Dystrophy.International journal of molecular sciences · 2025Review
- A comprehensive spatiotemporal map of dystrophin isoform expression in the developing and adult human brain.Acta neuropathologica communications · 2025Article
- Angiopoietin 1 Attenuates Dysregulated Angiogenesis in the Gastrocnemius of DMD Mice.International journal of molecular sciences · 2024Article
- Review
- Poor bone health in Duchenne muscular dystrophy: a multifactorial problem beyond corticosteroids and loss of ambulation.Frontiers in endocrinology · 2024Review
- Cellular interactions and microenvironment dynamics in skeletal muscle regeneration and disease.Frontiers in cell and developmental biology · 2024Review
- NTPDase1/CD39 Ectonucleotidase Is Necessary for Normal Arterial Diameter Adaptation to Flow.International journal of molecular sciences · 2023Article
- Article
- Cilostazol attenuates oxidative stress and apoptosis in the quadriceps muscle of the dystrophic mouse experimental model.International journal of experimental pathology · 2023Article
- Editorial: Molecular physiology of smooth muscle cells.Frontiers in physiology · 2023Article
- The importance of dystrophin and the dystrophin associated proteins in vascular smooth muscle.Frontiers in physiology · 2022Review
- Biofabrication of 3D Human Muscle Model with Vascularization and Endomysium.Methods in molecular biology (Clifton, N.J.) · 2022Article
- Dystrophin deficiency impairs vascular structure and function in the canine model of Duchenne muscular dystrophy.The Journal of pathology · 2021Article
- Influence of Different Types of Corticosteroids on Heart Rate Variability of Individuals with Duchenne Muscular Dystrophy-A Pilot Cross Sectional Study.Life (Basel, Switzerland) · 2021Article
Corrections and comments
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Authors and funding
7 authors at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
objectiveMutations in the dystrophin gene causing Duchenne's muscular dystrophy (DMD) lead to premature stop codons. In mice lacking dystrophin (mdx mice), a model for DMD, these mutations can be suppressed by aminoglycosides such as gentamicin. Dystrophin plays a role in flow (shear stress)-mediated endothelium-dependent dilation (FMD) in arteries. We investigated the effect of gentamicin on vascular contractile and dilatory functions, vascular structure, and density in mdx mice. METHODS AND
resultsIsolated mice carotid and mesenteric resistance arteries were mounted in arteriographs allowing continuous diameter measurements. Mdx mice showed lower nitric oxide (NO)-dependent FMD and endothelial NO synthase (eNOS) expression as well as decreased vascular density in gracilis and cardiac muscles compared with control mice. Treatment with gentamycin restored these parameters. In contrast, smooth muscle-dependent contractions as well as endothelium-dependent or -independent dilation were not affected by dystrophin deficiency or by gentamicin treatment.
conclusionsDystrophin deficiency induces a selective defect in flow-dependent mechanotransduction, thus attenuating FMD and eNOS expression, and may contribute to low arteriolar density. These findings open important perspectives regarding the mechanism involved in the pathophysiology of genetic diseases related to premature stop codons such as DMD.
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