ArticleJournal of molecular and cellular cardiology2015
Crosstalk between RyR2 oxidation and phosphorylation contributes to cardiac dysfunction in mice with Duchenne muscular dystrophy.
Article in Journal of molecular and cellular cardiology, 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 25 papers.
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Who cites it
25 citing papers in PubMed, 32 citations in OpenAlex.
- Adipocyte fatty acid-binding protein 4 suppresses contraction of mouse ventricular myocytes via a calcium-independent pathway.Frontiers in physiology · 2026Article
- Ryanodine receptor dysfunction causes senescence and fibrosis in Duchenne dilated cardiomyopathy.Journal of cachexia, sarcopenia and muscle · 2024Article
- 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
- Article
- The role of junctophilin proteins in cellular function.Physiological reviews · 2022Review
- Calcium handling maturation and adaptation to increased substrate stiffness in human iPSC-derived cardiomyocytes: The impact of full-length dystrophin deficiency.Frontiers in physiology · 2022Article
- Cardiac Myoediting Attenuates Cardiac Abnormalities in Human and Mouse Models of Duchenne Muscular Dystrophy.Circulation research · 2021Article
- Article
- Cardioprotective Effect of Whole Body Periodic Acceleration in Dystrophic PhenotypeFrontiers in physiology · 2021Article
- Inhibition of Autophagy Prevents Panax Notoginseng Saponins (PNS) Protection on Cardiac Myocytes Against Endoplasmic Reticulum (ER) Stress-Induced Mitochondrial Injury, CaFrontiers in pharmacology · 2021Article
- Abnormal Calcium Handling in Duchenne Muscular Dystrophy: Mechanisms and Potential Therapies.Frontiers in physiology · 2021Review
- Prevention of connexin-43 remodeling protects against Duchenne muscular dystrophy cardiomyopathy.The Journal of clinical investigation · 2020Article
- Quantitative tests reveal that microtubules tune the healthy heart but underlie arrhythmias in pathology.The Journal of physiology · 2020Article
- 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
- Cardiac-specific ablation of glutaredoxin 3 leads to cardiac hypertrophy and heart failure.Physiological reports · 2019Article
- Exacerbation of dystrophic cardiomyopathy by phospholamban deficiency mediated chronically increased cardiac CaAmerican journal of physiology. Heart and circulatory physiology · 2018Article
- Oxidized CaMKII (CaCirculation. Arrhythmia and electrophysiology · 2018Article
- Ryanodine channel complex stabilizer compound S48168/ARM210 as a disease modifier in dystrophin-deficient mdx mice: proof-of-concept study and independent validation of efficacy.FASEB journal : official publication of the Federation of American Societies for Experimental Biology · 2018Article
- Redox Dependent Modifications of Ryanodine Receptor: Basic Mechanisms and Implications in Heart Diseases.Frontiers in physiology · 2018Review
Corrections and comments
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Authors and funding
5 authors at 1 institution in 1 country.
Funding
Abstract
backgroundPatients with Duchenne muscular dystrophy (DMD) are at risk of developing cardiomyopathy and cardiac arrhythmias. Studies in a mouse model of DMD revealed that enhanced sarcoplasmic reticulum (SR) Ca(2+) leak contributes to the pathogenesis of cardiac dysfunction. In view of recent data suggesting the involvement of altered phosphorylation and oxidation of the cardiac ryanodine receptor (RyR2)/Ca(2+) release channel, we hypothesized that inhibition of RyR2 phosphorylation in a mouse model of DMD can prevent SR Ca(2+) leak by reducing RyR2 oxidation. METHODS AND
resultsConfocal Ca(2+) imaging and single RyR2 channel recordings revealed that both inhibition of S2808 or S2814 phosphorylation, and inhibition of oxidation could normalize RyR2 activity in mdx mice. Moreover, Western blotting revealed that genetic inhibition of RyR2 phosphorylation at S2808 or S2814 reduced RyR2 oxidation. Production of reactive oxygen species (ROS) in myocytes from mdx mice was reduced by both inhibition of RyR2 phosphorylation or the ROS scavenger 2-mercaptopropionyl glycine (MPG). Finally, it was shown that ROS production in mdx mice is proportional to the activity of RyR2-mediated SR Ca(2+) leak, and likely generated by Nox2.
conclusionsIncreased ROS production in the hearts of mdx mice drives the progression of cardiac dysfunction. Inhibition of RyR2 phosphorylation can suppress SR Ca(2+) leak in mdx mouse hearts in part by reducing RyR2 oxidation.
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