ArticleBiochemical and biophysical research communications2014
Age-dependent changes in diastolic Ca(2+) and Na(+) concentrations in dystrophic cardiomyopathy: Role of Ca(2+) entry and IP3.
Article in Biochemical and biophysical research communications, 2014. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 29 papers.
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Who cites it
29 citing papers in PubMed, 35 citations in OpenAlex.
- Neuronal hyperexcitability in dystrophin-deficient mdx hippocampal neurons: the importance of interleukin-6 and GABAergic regulation.Scientific reports · 2025Article
- Review
- 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
- The role of the dystrophin glycoprotein complex in muscle cell mechanotransduction.Communications biology · 2022Review
- The Role of the NaFrontiers in cellular and infection microbiology · 2022Article
- Effects of Sarcolemmal Background CaFrontiers in physiology · 2022Article
- Disrupted Calcium Homeostasis in Duchenne Muscular Dystrophy: A Common Mechanism behind Diverse Consequences.International journal of molecular sciences · 2021Review
- Article
- Molecular Modification of Transient Receptor Potential Canonical 6 Channels Modulates Calcium Dyshomeostasis in a Mouse Model Relevant to Malignant Hyperthermia.Anesthesiology · 2021Article
- Current Pharmacological Strategies for Duchenne Muscular Dystrophy.Frontiers in cell and developmental biology · 2021Review
- Cardioprotective Effect of Whole Body Periodic Acceleration in Dystrophic PhenotypeFrontiers in physiology · 2021Article
- Effects of Naringin on Cardiomyocytes From a Rodent Model of Type 2 Diabetes.Frontiers in pharmacology · 2021Article
- The Endothelium as a Therapeutic Target in Diabetes: A Narrative Review and Perspective.Frontiers in physiology · 2021Review
- Increases in [IP3]i aggravates diastolic [Ca2+] and contractile dysfunction in Chagas' human cardiomyocytes.PLoS neglected tropical diseases · 2020Article
- The Control of Diastolic Calcium in the Heart: Basic Mechanisms and Functional Implications.Circulation research · 2020Review
- Anti-Contractile and Anti-Inflammatory Effects of Diacerein on Isolated Mouse Airways Smooth Muscle and Mouse Asthma Model.Frontiers in pharmacology · 2020Article
- Contribution of TRPC Channels to Intracellular CaFrontiers in physiology · 2020Article
- Senescence Is Associated With Elevated Intracellular Resting [CaFrontiers in physiology · 2020Article
- DP71 and SERCA2 alteration in human neurons of a Duchenne muscular dystrophy patient.Stem cell research & therapy · 2019Article
- Quantum Blue Reduces the Severity of Woody Breast Myopathy via Modulation of Oxygen Homeostasis-Related Genes in Broiler Chickens.Frontiers in physiology · 2019Article
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Authors and funding
5 authors at 3 institutions in 2 countries.
Funding
Abstract
Duchenne muscular dystrophy (DMD) is a lethal X-inherited disease caused by dystrophin deficiency. Besides the relatively well characterized skeletal muscle degenerative processes, DMD is also associated with a dilated cardiomyopathy that leads to progressive heart failure at the end of the second decade. The aim of the present study was to characterize the diastolic Ca(2+) concentration ([Ca(2+)]d) and diastolic Na(+) concentration ([Na(+)]d) abnormalities in cardiomyocytes isolated from 3-, 6-, 9-, and 12-month old mdx mice using ion-selective microelectrodes. In addition, the contributions of gadolinium (Gd(3+))-sensitive Ca(2+) entry and inositol triphosphate (IP3) signaling pathways in abnormal [Ca(2+)]d and [Na(+)]d were investigated. Our results showed an age-dependent increase in both [Ca(2+)]d and [Na(+)]d in dystrophic cardiomyocytes compared to those isolated from age-matched wt mice. Gd(3+) treatment significantly reduced both [Ca(2+)]d and [Na(+)]d at all ages. In addition, blockade of the IP3-pathway with either U-73122 or xestospongin C significantly reduced ion concentrations in dystrophic cardiomyocytes. Co-treatment with U-73122 and Gd(3+) normalized both [Ca(2+)]d and [Na(+)]d at all ages in dystrophic cardiomyocytes. These data showed that loss of dystrophin in mdx cardiomyocytes produced an age-dependent intracellular Ca(2+) and Na(+) overload mediated at least in part by enhanced Ca(2+) entry through Gd(3+) sensitive transient receptor potential channels (TRPC), and by IP3 receptors.
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