ArticleThe American journal of pathology2005
A multidisciplinary evaluation of the effectiveness of cyclosporine a in dystrophic mdx mice.
Article in The American journal of pathology, 2005. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 42 papers.
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Who cites it
42 citing papers in PubMed, 129 citations in OpenAlex.
- Downstream Pathways of Dystrophin Deficiency in Duchenne Muscular Dystrophy: Implications for Muscle Degeneration and Regeneration.Journal of cachexia, sarcopenia and muscle · 2026Review
- Review
- Growth hormone secretagogues modulate inflammation and fibrosis inFrontiers in immunology · 2023Article
- Long-term maintenance of dystrophin expression and resistance to injury of skeletal muscle in gene edited DMD mice.Molecular therapy. Nucleic acids · 2022Article
- Alteration of STIM1/Orai1-Mediated SOCE in Skeletal Muscle: Impact in Genetic Muscle Diseases and Beyond.Cells · 2021Review
- Muscular dystrophy: Experimental animal models and therapeutic approaches (Review).Experimental and therapeutic medicine · 2021Review
- Review
- Beneficial Role of Exercise in the Modulation ofAntioxidants (Basel, Switzerland) · 2021Review
- Statin-Induced Myopathy: Translational Studies from Preclinical to Clinical Evidence.International journal of molecular sciences · 2021Review
- Zidovudine ameliorates pathology in the mouse model of Duchenne muscular dystrophy via P2RX7 purinoceptor antagonism.Acta neuropathologica communications · 2018Article
- Ryanodine channel complex stabilizer compound S48168/ARM210 as a disease modifier in dystrophin-deficient mdx mice: proof-of-concept study and independent validation of efficacy.FASEB journal : official publication of the Federation of American Societies for Experimental Biology · 2018Article
- Degenerative and regenerative features of myofibers differ among skeletal muscles in a murine model of muscular dystrophy.Journal of muscle research and cell motility · 2016Article
- Pharmacological therapeutics targeting the secondary defects and downstream pathology of Duchenne muscular dystrophy.Expert opinion on orphan drugs · 2016Article
- Comparison of Experimental Protocols of Physical Exercise for mdx Mice and Duchenne Muscular Dystrophy Patients.Journal of neuromuscular diseases · 2015Article
- Naproxcinod shows significant advantages over naproxen in the mdx model of Duchenne Muscular Dystrophy.Orphanet journal of rare diseases · 2015Article
- Angiotensin II modulates mouse skeletal muscle resting conductance to chloride and potassium ions and calcium homeostasis via the AT1 receptor and NADPH oxidase.American journal of physiology. Cell physiology · 2014Article
- Cyclosporin A Promotes in vivo Myogenic Response in Collagen VI-Deficient Myopathic Mice.Frontiers in aging neuroscience · 2014Article
- Andrographolide attenuates skeletal muscle dystrophy in mdx mice and increases efficiency of cell therapy by reducing fibrosis.Skeletal muscle · 2014Article
- Long-term wheel running compromises diaphragm function but improves cardiac and plantarflexor function in the mdx mouse.Journal of applied physiology (Bethesda, Md. : 1985) · 2013Article
- Microdystrophin ameliorates muscular dystrophy in the canine model of duchenne muscular dystrophy.Molecular therapy : the journal of the American Society of Gene Therapy · 2013Article
Corrections and comments
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Authors and funding
20 authors at 5 institutions in 3 countries.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Chronic inflammation is a secondary reaction of Duchenne muscular dystrophy and may contribute to disease progression. To examine whether immunosuppressant therapies could benefit dystrophic patients, we analyzed the effects of cyclosporine A (CsA) on a dystrophic mouse model. Mdx mice were treated with 10 mg/kg of CsA for 4 to 8 weeks throughout a period of exercise on treadmill, a protocol that worsens the dystrophic condition. The CsA treatment fully prevented the 60% drop of forelimb strength induced by exercise. A significant amelioration (P < 0.05) was observed in histological profile of CsA-treated gastrocnemius muscle with reductions of nonmuscle area (20%), centronucleated fibers (12%), and degenerating area (50%) compared to untreated exercised mdx mice. Consequently, the percentage of normal fibers increased from 26 to 35% in CsA-treated mice. Decreases in creatine kinase and markers of fibrosis were also observed. By electrophysiological recordings ex vivo, we found that CsA counteracted the decrease in chloride conductance (gCl), a functional index of degeneration in diaphragm and extensor digitorum longus muscle fibers. However, electrophysiology and fura-2 calcium imaging did not show any amelioration of calcium homeostasis in extensor digitorum longus muscle fibers. No significant effect was observed on utrophin levels in diaphragm muscle. Our data show that the CsA treatment significantly normalized many functional, histological, and biochemical endpoints by acting on events that are independent or downstream of calcium homeostasis. The beneficial effect of CsA may involve different targets, reinforcing the usefulness of immunosuppressant drugs in muscular dystrophy.
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