The primary disturbance in Duchenne muscular dystrophy (DMD) appears to affect membrane function, and changes characteristic of oxidant-induced damage occur in skeletal muscle and erythrocytes. There is recent evidence that DMD is a functional tocopherol deficiency, with reduced levels of the lipoprotein required to carry tocopherol to tissues. This may explain the parallels between DMD and dietary tocopherol deficiency. Thus DMD should follow the usual experience of other examples of oxidative pathology, where the balance between tocopherol, the main antioxidant in membrane lipids, and non protein-bound iron, an important catalyst of reactions which produce oxidizing free radicals, largely determines whether or not tissue damage occurs. Desferrioxamine prevents oxidant damage in vitro and in vivo by removing this iron, and may therefore be able to reverse the muscle damage of DMD. Recent experience with this drug in long term dialysis patients is consistent with this suggestion.
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http://dx.doi.org/10.1016/0306-9877(84)90026-4 | DOI Listing |
Muscle Nerve
January 2025
Department of Anatomy, Federal University of Alfenas (UNIFAL-MG), Alfenas, Brazil.
Introduction/aims: Duchenne muscular dystrophy (DMD) is caused by pathogenic variants in the DMD gene, making muscle fibers susceptible to contraction-induced membrane damage. Given the potential beneficial action of cannabidiol (CBD), we evaluated the in vitro effect of full-spectrum CBD oil on the viability of dystrophic muscle fibers and the in vivo effect on myopathy of the mdx mouse, a DMD model.
Methods: In vitro, dystrophic cells from the mdx mouse were treated with full-spectrum CBD oil and assessed with cell viability and cytotoxic analyses.
Clin Pharmacol Drug Dev
January 2025
Taiho Pharmaceutical Co., Ltd., Tokyo, Japan.
Pizuglanstat is a novel hematopoietic prostaglandin D synthase inhibitor and investigational treatment for Duchenne muscular dystrophy. This Phase 1 mass balance study aimed to characterize the absorption, metabolism, and excretion of carbon-14 (C)-labeled pizuglanstat in healthy adults (ClinicalTrials.gov, NCT04825431).
View Article and Find Full Text PDFFront Vet Sci
January 2025
Department of Veterinary Integrative Biosciences, Texas A&M University, College Station, TX, United States.
Duchenne muscular dystrophy (DMD) is an X-linked muscle disease with weakness, loss of ambulation, and premature death. DMD patients have reduced bone health, including decreased femur length (FL), density, and fractures. The mouse model has paradoxically greater FL, density, and strength, positively correlating with muscle mass.
View Article and Find Full Text PDFFront Psychol
January 2025
Pediatric Neuroscience Unit, IRCCS Mondino Foundation, Pavia, Italy.
Front Cell Dev Biol
January 2025
Department of Human Genetics, Leiden University Medical Center (LUMC), Leiden, Netherlands.
Muscle repair and regeneration are complex processes. In Duchenne muscular dystrophy (DMD), these processes are disrupted by the loss of functional dystrophin, a key part of the transmembrane dystrophin-associated glycoprotein complex that stabilizes myofibers, indirectly leading to progressive muscle wasting, subsequent loss of ambulation, respiratory and cardiac insufficiency, and premature death. As part of the DMD pathology, histone deacetylase (HDAC) activity is constitutively increased, leading to epigenetic changes and inhibition of muscle regeneration factors, chronic inflammation, fibrosis, and adipogenesis.
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