ArticleHuman molecular genetics2008
Molecular and cellular adaptations to chronic myotendinous strain injury in mdx mice expressing a truncated dystrophin.
Article in Human molecular genetics, 2008. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 24 papers.
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Who cites it
24 citing papers in PubMed, 43 citations in OpenAlex.
- Bidirectional role of Costameres in the pathophysiology of mdx skeletal muscles.Human molecular genetics · 2025Article
- Use of HSALab animal · 2025Article
- Alternative splicing dysregulation across tissue and therapeutic approaches in a mouse model of myotonic dystrophy type 1.Molecular therapy. Nucleic acids · 2024Article
- The Implication of Hinge 1 and Hinge 4 in Micro-Dystrophin Gene Therapy for Duchenne Muscular Dystrophy.Human gene therapy · 2023Article
- Duchenne muscular dystrophy: disease mechanism and therapeutic strategies.Frontiers in physiology · 2023Review
- Evolution and developmental functions of the dystrophin-associated protein complex: beyond the idea of a muscle-specific cell adhesion complex.Frontiers in cell and developmental biology · 2023Review
- Evaluation of the dystrophin carboxy-terminal domain for micro-dystrophin gene therapy in cardiac and skeletal muscles in the DMDGene therapy · 2022Article
- Microutrophin expression in dystrophic mice displays myofiber type differences in therapeutic effects.PLoS genetics · 2020Article
- Micro-dystrophin Gene Therapy Partially Enhances Exercise Capacity in Older AdultMolecular therapy. Methods & clinical development · 2020Article
- Development of Novel Micro-dystrophins with Enhanced Functionality.Molecular therapy : the journal of the American Society of Gene Therapy · 2019Article
- Cell death, clearance and immunity in the skeletal muscle.Cell death and differentiation · 2016Review
- The Dystrophin Complex: Structure, Function, and Implications for Therapy.Comprehensive Physiology · 2015Review
- Phosphorylation within the cysteine-rich region of dystrophin enhances its association with β-dystroglycan and identifies a potential novel therapeutic target for skeletal muscle wasting.Human molecular genetics · 2014Article
- Therapy of Genetic Disorders-Novel Therapies for Duchenne Muscular Dystrophy.Current pediatrics reports · 2014Article
- Muscle structure influences utrophin expression in mdx mice.PLoS genetics · 2014Article
- Successful regional delivery and long-term expression of a dystrophin gene in canine muscular dystrophy: a preclinical model for human therapies.Molecular therapy : the journal of the American Society of Gene Therapy · 2012Article
- Gene replacement therapies for duchenne muscular dystrophy using adeno-associated viral vectors.Current gene therapy · 2012Review
- NAD+ biosynthesis ameliorates a zebrafish model of muscular dystrophy.PLoS biology · 2012Article
- Gene therapy of mdx mice with large truncated dystrophins generated by recombination using rAAV6.Molecular therapy : the journal of the American Society of Gene Therapy · 2011Article
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Authors and funding
4 authors at 2 institutions in 1 country.
Funding
Abstract
Myotendinous strain injury is the most common injury of human skeletal muscles because the majority of muscle forces are transmitted through this region. Although the immediate response to strain injury is well characterized, the chronic response to myotendinous strain injury is less clear. Here we examined the molecular and cellular adaptations to chronic myotendinous strain injury in mdx mice expressing a microdystrophin transgene (microdystrophin(DeltaR4-R23)). We found that muscles with myotendinous strain injury had an increased expression of utrophin and alpha7-integrin together with the dramatic restructuring of peripheral myofibrils into concentric rings. The sarcolemma of the microdystrophin(DeltaR4-R23)/mdx gastrocnemius muscles was highly protected from experimental lengthening contractions, better than wild-type muscles. We also found a positive correlation between myotendinous strain injury and ringed fibers in the HSA(LR) (human skeletal actin, long repeat) mouse model of myotonic dystrophy. We suggest that changes in protein expression and the formation of rings are adaptations to myotendinous strain injury that help to prevent muscle necrosis and retain the function of necessary muscles during injury, ageing and disease.
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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.