ArticleJournal of molecular and cellular cardiology2014
Intracellular Na+ overload causes oxidation of CaMKII and leads to Ca2+ mishandling in isolated ventricular myocytes.
Article in Journal of molecular and cellular cardiology, 2014. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 37 papers.
What it found
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The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
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Who cites it
37 citing papers in PubMed, 55 citations in OpenAlex.
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- Multi-faceted potential of sophoridine compound's anti-arrhythmic and antioxidant effects through ROS/CaMKII pathway.Heliyon · 2024Article
- CaMK II in Cardiovascular Diseases, Especially CaMK II-δ: Friends or Enemies.Drug design, development and therapy · 2024Review
- The inotropic and arrhythmogenic effects of acutely increased late IFrontiers in cardiovascular medicine · 2024Article
- Ketogenic Diet Regulates Cardiac Remodeling and Calcium Homeostasis in Diabetic Rat Cardiomyopathy.International journal of molecular sciences · 2023Article
- Distinct Effects of Mitochondrial NaJournal of the American Heart Association · 2023Article
- Effect of macrophage migration inhibitory factor on pulmonary vein arrhythmogenesis through late sodium current.Europace : European pacing, arrhythmias, and cardiac electrophysiology : journal of the working groups on cardiac pacing, arrhythmias, and cardiac cellular electrophysiology of the European Society of Cardiology · 2023Article
- Calcium and Reactive Oxygen Species Signaling Interplays in Cardiac Physiology and Pathologies.Antioxidants (Basel, Switzerland) · 2023Review
- Advanced glycation end products modulate electrophysiological remodeling of right ventricular outflow tract cardiomyocytes: A novel target for diabetes-related ventricular arrhythmogenesis.Physiological reports · 2022Article
- Ziprasidone Induces Rabbit Atrium Arrhythmogenesis via Modification of Oxidative Stress and Sodium/Calcium Homeostasis.Biomedicines · 2022Article
- The Oxidative Balance Orchestrates the Main Keystones of the Functional Activity of Cardiomyocytes.Oxidative medicine and cellular longevity · 2022Review
- Benefits of SGLT2 inhibitors in arrhythmias.Frontiers in cardiovascular medicine · 2022Review
- Ranolazine: An Old Drug with Emerging Potential; Lessons from Pre-Clinical and Clinical Investigations for Possible Repositioning.Pharmaceuticals (Basel, Switzerland) · 2021Review
- Cardiomyocyte NaBasic research in cardiology · 2021Article
- Cardioprotection by SGLT2 Inhibitors-Does It All Come Down to NaInternational journal of molecular sciences · 2021Review
- The role of calcium homeostasis remodeling in inherited cardiac arrhythmia syndromes.Pflugers Archiv : European journal of physiology · 2021Review
- Fibroblast Growth Factor 1 Reduces Pulmonary Vein and Atrium ArrhythmogenesisFrontiers in cardiovascular medicine · 2021Article
- Mitochondrial Dysfunction Increases Arrhythmic Triggers and Substrates; Potential Anti-arrhythmic Pharmacological Targets.Frontiers in cardiovascular medicine · 2021Review
- Phosphoproteomic analysis identifies phospho-Threonine-17 site of phospholamban important in low molecular weight isoform of fibroblast growth factor 2-induced protection against post-ischemic cardiac dysfunction.Journal of molecular and cellular cardiology · 2020Article
- The effect of Sirt1 deficiency on CaJournal of cellular and molecular medicine · 2020Article
Corrections and comments
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Authors and funding
12 authors at 3 institutions in 1 country.
Funding
Abstract
An increase of late Na(+) current (INaL) in cardiac myocytes can raise the cytosolic Na(+) concentration and is associated with activation of Ca(2+)/calmodulin-dependent protein kinase II (CaMKII) and alterations of mitochondrial metabolism and Ca(2+) handling by sarcoplasmic reticulum (SR). We tested the hypothesis that augmentation of INaL can increase mitochondrial reactive oxygen species (ROS) production and oxidation of CaMKII, resulting in spontaneous SR Ca(2+) release and increased diastolic Ca(2+) in myocytes. Increases of INaL and/or of the cytosolic Na(+) concentration led to mitochondrial ROS production and oxidation of CaMKII to cause dysregulation of Ca(2+) handling in rabbit cardiac myocytes.
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Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.