ArticlePhysiological reports2019
Simvastatin provides long-term improvement of left ventricular function and prevents cardiac fibrosis in muscular dystrophy.
Article in Physiological reports, 2019. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 22 papers, 1 of them a synthesis that pooled it.
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Who cites it
22 citing papers in PubMed, 1 synthesis or guideline pooled it, 29 citations in OpenAlex.
- Muscle and cardiac therapeutic strategies for Duchenne muscular dystrophy: past, present, and future.Pharmacological reports : PR · 2020Pooled it
- Metabolic Complications and Ultrasound-Detected Liver Abnormalities in Paediatric Patients With Duchenne Muscular Dystrophy.Pediatric obesity · 2026Article
- Skeletal muscle disorders as risk factors for type 2 diabetes.Molecular and cellular endocrinology · 2025Review
- Statins-Beyond Their Use in Hypercholesterolemia: Focus on the Pediatric Population.Children (Basel, Switzerland) · 2024Review
- Calcium handling dysfunction and cardiac damage following acute ventricular preload challenge in the dystrophin-deficient mouse heart.American journal of physiology. Heart and circulatory physiology · 2023Article
- A Brief Review of Duchenne Muscular Dystrophy Treatment Options, with an Emphasis on Two Novel Strategies.Biomedicines · 2023Review
- Vascular therapy for Duchenne muscular dystrophy (DMD).Faculty reviews · 2023Review
- Duchenne muscular dystrophy: disease mechanism and therapeutic strategies.Frontiers in physiology · 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
- Upregulation of Wilms' Tumor 1 in epicardial cells increases cardiac fibrosis in dystrophic mice.Cell death and differentiation · 2022Article
- Statins in High Cardiovascular Risk Patients: Do Comorbidities and Characteristics Matter?International journal of molecular sciences · 2022Review
- Deciphering the Molecular Mechanism of Incurable Muscle Disease by a Novel Method for the Interpretation of miRNA Dysregulation.Non-coding RNA · 2022Article
- Cardiovascular Disease in Duchenne Muscular Dystrophy: Overview and Insight Into Novel Therapeutic Targets.JACC. Basic to translational science · 2022Review
- 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 does not alleviate muscle pathology in a mouse model of Duchenne muscular dystrophy.Skeletal muscle · 2021Article
- Micro-dystrophin gene therapy prevents heart failure in an improved Duchenne muscular dystrophy cardiomyopathy mouse model.JCI insight · 2021Article
- Simvastatin Treatment Does Not Ameliorate Muscle Pathophysiology in a Mouse Model for Duchenne Muscular Dystrophy.Journal of neuromuscular diseases · 2021Article
- Statin use in patients with non-HMGCR idiopathic inflammatory myopathies: A retrospective study.Clinical cardiology · 2020Article
- Teaching an Old Molecule New Tricks: Drug Repositioning for Duchenne Muscular Dystrophy.International journal of molecular sciences · 2019Review
- Cardiac Pathophysiology and the Future of Cardiac Therapies in Duchenne Muscular Dystrophy.International journal of molecular sciences · 2019Review
Corrections and comments
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Authors and funding
6 authors at 1 institution in 1 country.
Funding
Abstract
Duchenne muscular dystrophy (DMD), caused by absence of the protein dystrophin, is a common, degenerative muscle disease affecting 1:5000 males worldwide. With recent advances in respiratory care, cardiac dysfunction now accounts for 50% of mortality in DMD. Recently, we demonstrated that simvastatin substantially improved skeletal muscle health and function in mdx (DMD) mice. Given the known cardiovascular benefits ascribed to statins, the aim of this study was to evaluate the efficacy of simvastatin on cardiac function in mdx mice. Remarkably, in 12-month old mdx mice, simvastatin reversed diastolic dysfunction to normal after short-term treatment (8 weeks), as measured by echocardiography in animals anesthetized with isoflurane and administered dobutamine to maintain a physiological heart rate. This improvement in diastolic function was accompanied by increased phospholamban phosphorylation in simvastatin-treated mice. Echocardiography measurements during long-term treatment, from 6 months up to 18 months of age, showed that simvastatin significantly improved in vivo cardiac function compared to untreated mdx mice, and prevented fibrosis in these very old animals. Cardiac dysfunction in DMD is also characterized by decreased heart rate variability (HRV), which indicates autonomic function dysregulation. Therefore, we measured cardiac ECG and demonstrated that short-term simvastatin treatment significantly increased heart rate variability (HRV) in 14-month-old conscious mdx mice, which was reversed by atropine. This finding suggests that enhanced parasympathetic function is likely responsible for the improved HRV mediated by simvastatin. Together, these findings indicate that simvastatin markedly improves cardiac health and function in dystrophic mice, and therefore may provide a novel approach for treating cardiomyopathy in DMD.
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