ArticleJournal of orthopaedic research : official publication of the Orthopaedic Research Society2013
Dystrophin and utrophin "double knockout" dystrophic mice exhibit a spectrum of degenerative musculoskeletal abnormalities.
Article in Journal of orthopaedic research : official publication of the Orthopaedic Research Society, 2013. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 37 papers.
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Who cites it
37 citing papers in PubMed, 60 citations in OpenAlex.
- Targeting cellular senescence in dystrophinPharmacological research · 2025Article
- Extracellular matrix: Dystroglycan interactions-Roles for the dystrophin-associated glycoprotein complex in skeletal tissue dynamics.International journal of experimental pathology · 2025Review
- Article
- Two Novel Mouse Models of Duchenne Muscular Dystrophy with Similar Dmd Exon 51 Frameshift Mutations and Varied Phenotype Severity.International journal of molecular sciences · 2024Article
- Circadian Clock in Muscle Disease Etiology and Therapeutic Potential for Duchenne Muscular Dystrophy.International journal of molecular sciences · 2024Review
- A causative role for periarticular skeletal muscle weakness in the progression of joint damage and pain in OA.Scientific reports · 2023Article
- Resolution of fibrosis in mdx dystrophic mouse after oral consumption of N-163 strain of Aureobasidium pullulans produced β-glucan.Scientific reports · 2023Article
- Review
- Assessment of the Impact of Physical Activity on the Musculoskeletal System in Early Degenerative Knee Joint Lesions in an Animal Model.International journal of molecular sciences · 2023Article
- Selective ablation of Nfix in macrophages attenuates muscular dystrophy by inhibiting fibro-adipogenic progenitor-dependent fibrosis.The Journal of pathology · 2022Article
- Articular cartilage degeneration and bone adaptation due to lack of dystrophin in mice.Journal of bone and mineral metabolism · 2022Article
- Partial Ablation of Non-Myogenic Progenitor Cells as a Therapeutic Approach to Duchenne Muscular Dystrophy.Biomolecules · 2021Article
- Accelerating theLife (Basel, Switzerland) · 2021Article
- Therapeutic aspects of cell signaling and communication in Duchenne muscular dystrophy.Cellular and molecular life sciences : CMLS · 2021Review
- Improved Bone Quality and Bone Healing of Dystrophic Mice by Parabiosis.Metabolites · 2021Article
- Recent Trends in Biofabrication Technologies for Studying Skeletal Muscle Tissue-Related Diseases.Frontiers in bioengineering and biotechnology · 2021Review
- Article
- Morpholino Oligomer-Induced Dystrophin Isoforms to Map the Functional Domains in the Dystrophin Protein.Molecular therapy. Nucleic acids · 2020Article
- Article
- Increased Expression of FGF-21 Negatively Affects Bone Homeostasis in Dystrophin/Utrophin Double Knockout Mice.Journal of bone and mineral research : the official journal of the American Society for Bone and Mineral Research · 2020Article
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Authors and funding
12 authors at 1 institution in 1 country.
Funding
Abstract
Duchenne muscular dystrophy (DMD) is a degenerative muscle disorder characterized by the lack of dystrophin expression at the sarcolemma of muscle fibers. In addition, DMD patients acquire osteopenia, fragility fractures, and scoliosis indicating that a deficiency in skeletal homeostasis coexists but little is known about the effects of DMD on bone and other connective tissues within the musculoskeletal system. Recent evidence has emerged implicating adult stem cell dysfunction in DMD myopathogenesis. Given the common mesenchymal origin of muscle and bone, we sought to investigate bone and other musculoskeletal tissues in a DMD mouse model. Here, we report that dystrophin-utrophin double knockout (dko) mice exhibit a spectrum of degenerative changes, outside skeletal muscle, in bone, articular cartilage, and intervertebral discs, in addition to reduced lifespan, muscle degeneration, spinal deformity, and cardiomyopathy previously reported. We also report these mice to have a reduced capacity for bone healing and exhibit spontaneous heterotopic ossification in the hind limb muscles. Therefore, we propose the dko mouse as a model for premature musculoskeletal aging and posit that a similar phenomenon may occur in patients with DMD.
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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.