ArticleInternational journal of cardiology2016
Ryanodine receptor phosphorylation by CaMKII promotes spontaneous Ca(2+) release events in a rodent model of early stage diabetes: The arrhythmogenic substrate.
Article in International journal of cardiology, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 37 papers.
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Who cites it
37 citing papers in PubMed, 59 citations in OpenAlex.
- Sirtuin signalling governs calcium homeostasis and mitochondrial function in metabolic syndrome cardiomyocytes.Experimental physiology · 2026Article
- Berberine Stabilizes the Arrhythmogenic Substrate in Obese Rats by Klotho-Mediated Attenuation of Oxidative Stress and Inflammation.International journal of molecular sciences · 2026Article
- Shengmai San Ameliorates High-Glucose-Induced Calcium Homeostasis Imbalance via Improving Energy Metabolism in Neonatal Rat Cardiomyocytes.Pharmaceuticals (Basel, Switzerland) · 2026Article
- Experimental Models for Studying Cardiovascular Dysfunction in Metabolic Syndrome.Handbook of experimental pharmacology · 2026Review
- Ablation of mitochondrial calcium uniporter alleviates cardiac dysfunction in type 1 diabetes.Cell calcium · 2026Article
- The role of stress hyperglycemia in in-hospital new-onset atrial fibrillation among patients with acute myocardial infarction: a narrative review.Frontiers in cardiovascular medicine · 2026Review
- Calcium Signaling and Cardiac Adaptation to Stress: Focus on Pregnancy and Diabetes.Biomolecules · 2025Review
- Mitochondrial Dysfunction in Arrhythmia and Cardiac Hypertrophy.Reviews in cardiovascular medicine · 2023Review
- Metabolic Syndrome and Atrial Fibrillation: Different Entities or Combined Disorders.Journal of personalized medicine · 2023Review
- The functions of CaJournal of cell communication and signaling · 2023Review
- The interplay of inflammation, exosomes and CaCardiovascular diabetology · 2023Review
- CardIAP: calcium transients confocal image analysis tool.Frontiers in bioinformatics · 2023Article
- STIM1-Orai1 interaction mediated calcium influx activation contributes to cardiac contractility of insulin-resistant rats.BMC cardiovascular disorders · 2022Article
- CaPflugers Archiv : European journal of physiology · 2022Review
- MOTS-c repairs myocardial damage by inhibiting the CCN1/ERK1/2/EGR1 pathway in diabetic rats.Frontiers in nutrition · 2022Article
- Hypochlorite-Modified LDL Induces Arrhythmia and Contractile Dysfunction in Cardiomyocytes.Antioxidants (Basel, Switzerland) · 2021Article
- Two-hit mechanism of cardiac arrhythmias in diabetic hyperglycaemia: reduced repolarization reserve, neurohormonal stimulation, and heart failure exacerbate susceptibility.Cardiovascular research · 2021Article
- Glycation and Glycosylation in Cardiovascular Remodeling: Focus on Advanced Glycation End Products and O-Linked Glycosylations as Glucose-Related Pathogenetic Factors and Disease Markers.Journal of clinical medicine · 2021Review
- Tale of two kinases: Protein kinase A and CaWorld journal of diabetes · 2021Review
- CaMKII activation in early diabetic hearts induces altered sarcoplasmic reticulum-mitochondria signaling.Scientific reports · 2021Article
Corrections and comments
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Authors and funding
10 authors at 5 institutions in 2 countries.
Funding
Abstract
backgroundHeart failure and arrhythmias occur more frequently in patients with type 2 diabetes (T2DM) than in the general population. T2DM is preceded by a prediabetic condition marked by elevated reactive oxygen species (ROS) and subclinical cardiovascular defects. Although multifunctional Ca2+ calmodulin-dependent protein kinase II (CaMKII) is ROS-activated and CaMKII hyperactivity promotes cardiac diseases, a link between prediabetes and CaMKII in the heart is unprecedented.
objectivesTo prove the hypothesis that increased ROS and CaMKII activity contribute to heart failure and arrhythmogenic mechanisms in early stage diabetes. METHODS-
resultsEchocardiography, electrocardiography, biochemical and intracellular Ca2+ (Ca2+i) determinations were performed in fructose-rich diet-induced impaired glucose tolerance, a prediabetes model, in rodents. Fructose-rich diet rats showed decreased contractility and hypertrophy associated with increased CaMKII activity, ROS production, oxidized CaMKII and enhanced CaMKII-dependent ryanodine receptor (RyR2) phosphorylation compared to rats fed with control diet. Isolated cardiomyocytes from fructose-rich diet showed increased spontaneous Ca2+i release events associated with spontaneous contractions, which were prevented by KN-93, a CaMKII inhibitor, or addition of Tempol, a ROS scavenger, to the diet. Moreover, fructose-rich diet myocytes showed increased diastolic Ca2+ during the burst of spontaneous Ca2+i release events. Mice treated with Tempol or with sarcoplasmic reticulum-targeted CaMKII-inhibition by transgenic expression of the CaMKII inhibitory peptide AIP, were protected from fructose-rich diet-induced spontaneous Ca2+i release events, spontaneous contractions and arrhythmogenesis in vivo, despite ROS increases.
conclusionsRyR2 phosphorylation by ROS-activated CaMKII, contributes to impaired glucose tolerance-induced arrhythmogenic mechanisms, suggesting that CaMKII inhibition could prevent prediabetic cardiovascular complications and/or evolution.
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