ArticlePloS one2011
Chronic losartan administration reduces mortality and preserves cardiac but not skeletal muscle function in dystrophic mice.
Article in PloS one, 2011. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 32 papers.
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Who cites it
32 citing papers in PubMed, 59 citations in OpenAlex.
- Vascular and musculoskeletal interactions: structure, function, and therapeutic strategies for sarcopenia and osteoporosis.MedScience · 2026Review
- Beta-hydroxy-beta-methylbutyrate (HMB) improves daily activity and whole-body protein metabolism in Duchenne muscular dystrophy dogs: a pilot study.Scientific reports · 2025Article
- (-)-Epicatechin Ameliorates Cardiac Fibrosis in a Female Rat Model of Pre-Heart Failure with Preserved Ejection Fraction.Journal of medicinal food · 2022Article
- Variations in native T1 values in patients with Duchenne muscular dystrophy with and without late gadolinium enhancement.The international journal of cardiovascular imaging · 2021Article
- Sarcolipin haploinsufficiency prevents dystrophic cardiomyopathy inAmerican journal of physiology. Heart and circulatory physiology · 2021Article
- Current Pharmacological Strategies for Duchenne Muscular Dystrophy.Frontiers in cell and developmental biology · 2021Review
- Role of the Renin-Angiotensin-Aldosterone System in Dystrophin-Deficient Cardiomyopathy.International journal of molecular sciences · 2020Review
- Losartan improves the therapeutic effect of metronomic cyclophosphamide in triple negative mammary cancer models.Oncotarget · 2020Article
- Anti-Inflammatory and General Glucocorticoid Physiology in Skeletal Muscles Affected by Duchenne Muscular Dystrophy: Exploration of Steroid-Sparing Agents.International journal of molecular sciences · 2020Review
- Update on Muscular Dystrophies with Focus on Novel Treatments and Biomarkers.Current neurology and neuroscience reports · 2020Review
- N-Acetyl-L-Cysteine Reduces Fibrosis and Improves Muscle Function After Acute Compartment Syndrome Injury.Military medicine · 2020Article
- Acute ATJournal of molecular and cellular cardiology · 2019Article
- Article
- Regulation of fibrosis in muscular dystrophy.Matrix biology : journal of the International Society for Matrix Biology · 2018Review
- The angiotensin receptor blocker, Losartan, inhibits mammary tumor development and progression to invasive carcinoma.Oncotarget · 2017Article
- Pharmacological therapeutics targeting the secondary defects and downstream pathology of Duchenne muscular dystrophy.Expert opinion on orphan drugs · 2016Article
- Clinical potential of ataluren in the treatment of Duchenne muscular dystrophy.Degenerative neurological and neuromuscular disease · 2016Review
- Current and emerging treatment strategies for Duchenne muscular dystrophy.Neuropsychiatric disease and treatment · 2016Review
- Angiotensin-dependent autonomic dysregulation precedes dilated cardiomyopathy in a mouse model of muscular dystrophy.Experimental physiology · 2015Article
- Myocardial fibrosis burden predicts left ventricular ejection fraction and is associated with age and steroid treatment duration in duchenne muscular dystrophy.Journal of the American Heart Association · 2015Article
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Authors and funding
8 authors at 2 institutions in 1 country.
Funding
Abstract
Duchenne muscular dystrophy (DMD) is a degenerative disorder affecting skeletal and cardiac muscle for which there is no effective therapy. Angiotension receptor blockade (ARB) has excellent therapeutic potential in DMD based on recent data demonstrating attenuation of skeletal muscle disease progression during 6-9 months of therapy in the mdx mouse model of DMD. Since cardiac-related death is major cause of mortality in DMD, it is important to evaluate the effect of any novel treatment on the heart. Therefore, we evaluated the long-term impact of ARB on both the skeletal muscle and cardiac phenotype of the mdx mouse. Mdx mice received either losartan (0.6 g/L) (n = 8) or standard drinking water (n = 9) for two years, after which echocardiography was performed to assess cardiac function. Skeletal muscle weight, morphology, and function were assessed. Fibrosis was evaluated in the diaphragm and heart by Trichrome stain and by determination of tissue hydroxyproline content. By the study endpoint, 88% of treated mice were alive compared to only 44% of untreated (p = 0.05). No difference in skeletal muscle morphology, function, or fibrosis was noted in losartan-treated animals. Cardiac function was significantly preserved with losartan treatment, with a trend towards reduction in cardiac fibrosis. We saw no impact on the skeletal muscle disease progression, suggesting that other pathways that trigger fibrosis dominate over angiotensin II in skeletal muscle long term, unlike the situation in the heart. Our study suggests that ARB may be an important prophylactic treatment for DMD-associated cardiomyopathy, but will not impact skeletal muscle disease.
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