ArticleProceedings of the National Academy of Sciences of the United States of America2010
Genetic inhibition of PKA phosphorylation of RyR2 prevents dystrophic cardiomyopathy.
Article in Proceedings of the National Academy of Sciences of the United States of America, 2010. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 40 papers.
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Who cites it
40 citing papers in PubMed, 52 citations in OpenAlex.
- Functional cardiac consequences of β-adrenergic stress-induced injury in a model of Duchenne muscular dystrophy.Disease models & mechanisms · 2024Article
- Review
- Functional cardiac consequences of β-adrenergic stress-induced injury in thebioRxiv : the preprint server for biology · 2024Article
- 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
- Targeting p21-activated kinase 1 for development of a novel anti-arrhythmic drug class.Philosophical transactions of the Royal Society of London. Series B, Biological sciences · 2023Review
- STAT3 in tumor fibroblasts promotes an immunosuppressive microenvironment in pancreatic cancer.Life science alliance · 2022Article
- The role of junctophilin proteins in cellular function.Physiological reviews · 2022Review
- Cardiovascular Disease in Duchenne Muscular Dystrophy: Overview and Insight Into Novel Therapeutic Targets.JACC. Basic to translational science · 2022Review
- CD38-NADase is a new major contributor to Duchenne muscular dystrophic phenotype.EMBO molecular medicine · 2022Article
- Targeting calcium-mediated inter-organellar crosstalk in cardiac diseases.Expert opinion on therapeutic targets · 2022Article
- Metabolic Alterations in Cardiomyocytes of Patients with Duchenne and Becker Muscular Dystrophies.Journal of clinical medicine · 2019Review
- Cardiac Pathophysiology and the Future of Cardiac Therapies in Duchenne Muscular Dystrophy.International journal of molecular sciences · 2019Review
- Voltage-Dependent Sarcolemmal Ion Channel Abnormalities in the Dystrophin-Deficient Heart.International journal of molecular sciences · 2018Review
- Calcium current properties in dystrophin-deficient ventricular cardiomyocytes from aged mdx mice.Physiological reports · 2018Article
- Deficit in PINK1/PARKIN-mediated mitochondrial autophagy at late stages of dystrophic cardiomyopathy.Cardiovascular research · 2018Article
- Force development and intracellular CaEuropean journal of pharmacology · 2017Article
- Regulation of sarcoplasmic reticulum CaJournal of molecular and cellular cardiology · 2016Review
- Connecting enterovirus infection to dystrophin dysfunction in dilated cardiomyopathy.Annals of translational medicine · 2016Article
- Microtubule-Mediated Misregulation of Junctophilin-2 Underlies T-Tubule Disruptions and Calcium Mishandling inJACC. Basic to translational science · 2016Article
- Crosstalk between RyR2 oxidation and phosphorylation contributes to cardiac dysfunction in mice with Duchenne muscular dystrophy.Journal of molecular and cellular cardiology · 2015Article
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Authors and funding
6 authors at 1 institution in 1 country.
Funding
Abstract
Aberrant intracellular Ca(2+) regulation is believed to contribute to the development of cardiomyopathy in Duchenne muscular dystrophy. Here, we tested whether inhibition of protein kinase A (PKA) phosphorylation of ryanodine receptor type 2 (RyR2) prevents dystrophic cardiomyopathy by reducing SR Ca(2+) leak in the mdx mouse model of Duchenne muscular dystrophy. mdx mice were crossed with RyR2-S2808A mice, in which PKA phosphorylation site S2808 on RyR2 is inactivated by alanine substitution. Compared with mdx mice that developed age-dependent heart failure, mdx-S2808A mice exhibited improved fractional shortening and reduced cardiac dilation. Whereas application of isoproterenol severely depressed cardiac contractility and caused 95% mortality in mdx mice, contractility was preserved with only 19% mortality in mdx-S2808A mice. SR Ca(2+) leak was greater in ventricular myocytes from mdx than mdx-S2808A mice. Myocytes from mdx mice had a higher incidence of isoproterenol-induced diastolic Ca(2+) release events than myocytes from mdx-S2808A mice. Thus, inhibition of PKA phosphorylation of RyR2 reduced SR Ca(2+) leak and attenuated cardiomyopathy in mdx mice, suggesting that enhanced PKA phosphorylation of RyR2 at S2808 contributes to abnormal Ca(2+) homeostasis associated with dystrophic cardiomyopathy.
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