ArticleSkeletal muscle2021
Simvastatin does not alleviate muscle pathology in a mouse model of Duchenne muscular dystrophy.
Article in Skeletal muscle, 2021. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 16 papers.
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Who cites it
16 citing papers in PubMed.
- Metabolic Complications and Ultrasound-Detected Liver Abnormalities in Paediatric Patients With Duchenne Muscular Dystrophy.Pediatric obesity · 2026Article
- TRPV1 manipulating polarization of M1/M2 macrophages to promote skeletal muscle regeneration.Skeletal muscle · 2026Article
- Cell therapy for Duchenne muscular dystrophy: promises, challenges, and controversies.Cellular and molecular life sciences : CMLS · 2025Review
- Effects of HMG CoA reductase (HMGCR) deficiency on skeletal muscle development.The FEBS journal · 2025Article
- Association between triglycerides and remnant cholesterol levels and spine bone mineral density in Duchenne muscular dystrophy.Lipids in health and disease · 2025Article
- Skeletal muscle disorders as risk factors for type 2 diabetes.Molecular and cellular endocrinology · 2025Review
- Development of an LC-MS method for the determination of simvastatin and its hydroxy acid form in muscle tissue and method application.PloS one · 2025Article
- Statins-Beyond Their Use in Hypercholesterolemia: Focus on the Pediatric Population.Children (Basel, Switzerland) · 2024Review
- Is sarcopenia an associated factor of increased administration of specific medications in patients with heart failure? A systematic review and meta-analysis.Frontiers in cardiovascular medicine · 2024Review
- miR-378 influences muscle satellite cells and enhances adipogenic potential of fibro-adipogenic progenitors but does not affect muscle regeneration in the glycerol-induced injury model.Scientific reports · 2023Article
- Vascular therapy for Duchenne muscular dystrophy (DMD).Faculty reviews · 2023Review
- Limb-girdle muscular dystrophy type 2B causes HDL-C abnormalities in patients and statin-resistant muscle wasting in dysferlin-deficient mice.Skeletal muscle · 2022Article
- Cardio-respiratory and phenotypic rescue of dystrophin/utrophin-deficient mice by combination therapy.EMBO reports · 2022Article
- miR-378 affects metabolic disturbances in the mdx model of Duchenne muscular dystrophy.Scientific reports · 2022Article
- Co-Administration of Simvastatin Does Not Potentiate the Benefit of Gene Therapy in the mdx Mouse Model for Duchenne Muscular Dystrophy.International journal of molecular sciences · 2022Article
- Simvastatin and Muscle: Zebrafish and Chicken Show that the Benefits are not Worth the Damage.Frontiers in cell and developmental biology · 2022Article
Corrections and comments
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Authors and funding
6 authors.
Funding
No grant is acknowledged in the PubMed record.
Abstract
backgroundDuchenne muscular dystrophy (DMD) is an incurable disease, caused by the mutations in the DMD gene, encoding dystrophin, an actin-binding cytoskeletal protein. Lack of functional dystrophin results in muscle weakness, degeneration, and as an outcome cardiac and respiratory failure. As there is still no cure for affected individuals, the pharmacological compounds with the potential to treat or at least attenuate the symptoms of the disease are under constant evaluation. The pleiotropic agents, 3-hydroxy-3-methylglutaryl coenzyme A (HMG-CoA) reductase inhibitors, known as statins, have been suggested to exert beneficial effects in the mouse model of DMD. On the other hand, they were also reported to induce skeletal-muscle myopathy. Therefore, we decided to verify the hypothesis that simvastatin may be considered a potential therapeutic agent in DMD.
methodsSeveral methods including functional assessment of muscle function via grip strength measurement, treadmill test, and single-muscle force estimation, enzymatic assays, histological analysis of muscle damage, gene expression evaluation, and immunofluorescence staining were conducted to study simvastatin-related alterations in the mdx mouse model of DMD.
resultsIn our study, simvastatin treatment of mdx mice did not result in improved running performance, grip strength, or specific force of the single muscle. Creatine kinase and lactate dehydrogenase activity, markers of muscle injury, were also unaffected by simvastatin delivery in mdx mice. Furthermore, no significant changes in inflammation, fibrosis, and angiogenesis were noted. Despite the decreased percentage of centrally nucleated myofibers in gastrocnemius muscle after simvastatin delivery, no changes were noticed in other regeneration-related parameters. Of note, even an increased rate of necrosis was found in simvastatin-treated mdx mice.
conclusionIn conclusion, our study revealed that simvastatin does not ameliorate DMD pathology.
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