ArticleJournal of translational medicine2011
SERCA2a gene transfer improves electrocardiographic performance in aged mdx mice.
Article in Journal of translational medicine, 2011. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 34 papers, 1 of them a synthesis that pooled it.
What it found
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Who cites it
34 citing papers in PubMed, 1 synthesis or guideline pooled it, 49 citations in OpenAlex.
- Muscle and cardiac therapeutic strategies for Duchenne muscular dystrophy: past, present, and future.Pharmacological reports : PR · 2020Pooled it
- DWORF Gene Therapy Improves Cardiac Calcium Handling and Mitochondrial Function.Circulation research · 2025Article
- DWORF expression is reduced in a large animal model of Duchenne muscular dystrophy.Disease models & mechanisms · 2025Article
- Review
- SERCA2a overexpression improves muscle function in a canine Duchenne muscular dystrophy model.Molecular therapy. Methods & clinical development · 2024Article
- Inhibition of miR-25 ameliorates cardiac and skeletal muscle dysfunction in agedMolecular therapy. Nucleic acids · 2024Article
- Dwarf Open Reading Frame (DWORF) Gene Therapy Ameliorated Duchenne Muscular Dystrophy Cardiomyopathy in Aged mdx Mice.Journal of the American Heart Association · 2023Article
- Ion Channels of the Sarcolemma and Intracellular Organelles in Duchenne Muscular Dystrophy: A Role in the Dysregulation of Ion Homeostasis and a Possible Target for Therapy.International journal of molecular sciences · 2023Review
- Pharmacological activation of SERCA ameliorates dystrophic phenotypes in dystrophin-deficient mdx mice.Human molecular genetics · 2021Article
- Abnormal Calcium Handling in Duchenne Muscular Dystrophy: Mechanisms and Potential Therapies.Frontiers in physiology · 2021Review
- Sarcolipin haploinsufficiency prevents dystrophic cardiomyopathy inAmerican journal of physiology. Heart and circulatory physiology · 2021Article
- Single SERCA2a Therapy Ameliorated Dilated Cardiomyopathy for 18 Months in a Mouse Model of Duchenne Muscular Dystrophy.Molecular therapy : the journal of the American Society of Gene Therapy · 2020Article
- Dysregulation of Calcium Handling in Duchenne Muscular Dystrophy-Associated Dilated Cardiomyopathy: Mechanisms and Experimental Therapeutic Strategies.Journal of clinical medicine · 2020Review
- CTRP5-Overexpression Attenuated Ischemia-Reperfusion Associated Heart Injuries and Improved Infarction Induced Heart Failure.Frontiers in pharmacology · 2020Article
- Canine Models of Inherited Musculoskeletal and Neurodegenerative Diseases.Frontiers in veterinary science · 2020Review
- From Genome-Wide Association Studies to Cardiac Electrophysiology: Through the Maze of Biological Complexity.Frontiers in physiology · 2020Review
- Sarcolipin overexpression impairs myogenic differentiation in Duchenne muscular dystrophy.American journal of physiology. Cell physiology · 2019Article
- Exacerbation of dystrophic cardiomyopathy by phospholamban deficiency mediated chronically increased cardiac CaAmerican journal of physiology. Heart and circulatory physiology · 2018Article
- Correcting Calcium Dysregulation in Chronic Heart Failure Using SERCA2a Gene Therapy.International journal of molecular sciences · 2018Review
- Nanotherapy for Duchenne muscular dystrophy.Wiley interdisciplinary reviews. Nanomedicine and nanobiotechnology · 2018Review
Corrections and comments
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Authors and funding
5 authors at 2 institutions in 1 country.
Funding
Abstract
backgroundCardiomyocyte calcium overloading has been implicated in the pathogenesis of Duchenne muscular dystrophy (DMD) heart disease. The cardiac isoform of sarcoplasmic reticulum calcium ATPase (SERCA2a) plays a major role in removing cytosolic calcium during heart muscle relaxation. Here, we tested the hypothesis that SERCA2a over-expression may mitigate electrocardiography (ECG) abnormalities in old female mdx mice, a murine model of DMD cardiomyopathy.
methods1 × 10(12) viral genome particles/mouse of adeno-associated virus serotype-9 (AAV-9) SERCA2a vector was delivered to 12-m-old female mdx mice (N = 5) via a single bolus tail vein injection. AAV transduction and the ECG profile were examined eight months later.
resultsThe vector genome was detected in the hearts of all AAV-injected mdx mice. Immunofluorescence staining and western blot confirmed SERCA2a over-expression in the mdx heart. Untreated mdx mice showed characteristic tachycardia, PR interval reduction and QT interval prolongation. AAV-9 SERCA2a treatment corrected these ECG abnormalities.
conclusionsOur results suggest that AAV SERCA2a therapy may hold great promise in treating dystrophin-deficient heart disease.
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Registered trials
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