ArticleThe Journal of clinical investigation2021
Oxidized CaMKII and O-GlcNAcylation cause increased atrial fibrillation in diabetic mice by distinct mechanisms.
Article in The Journal of clinical investigation, 2021. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 50 papers, 2 of them syntheses that pooled it.
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Who cites it
50 citing papers in PubMed, 2 syntheses or guidelines pooled it, 76 citations in OpenAlex.
- 2023 ACC/AHA/ACCP/HRS Guideline for the Diagnosis and Management of Atrial Fibrillation: A Report of the American College of Cardiology/American Heart Association Joint Committee on Clinical Practice Guidelines.Journal of the American College of Cardiology · 2024Guideline
- Guideline
- Role of NADPH oxidase 2-derived reactive oxygen species in cardiac electrophysiological disorders.Channels (Austin, Tex.) · 2026Review
- PFKFB2 Gates a Relationship Between Cardiac Glycolytic Regulation and Electrophysiological Function.Circulation. Arrhythmia and electrophysiology · 2026Article
- The Deubiquitinase UCHL1 Drives Susceptibility to Atrial Fibrillation by Stabilizing CaMKII-δ.Advanced science (Weinheim, Baden-Wurttemberg, Germany) · 2026Article
- Orchestrating glucose metabolism: PFKFB2 as a signal-integrating conductor in homeostasis and disease.The Journal of biological chemistry · 2026Review
- The clinical pathophysiology of atrial fibrillation: outstanding questions from bedside to bench and back.Physiological reviews · 2026Review
- Atrial Fibrillation in Diabetes: Epidemiology, Mechanisms and Integrated Management.Journal of clinical medicine · 2026Review
- Mutation of a single cysteine in CaMKIIδ protects the heart from ischemia-reperfusion Injury.bioRxiv : the preprint server for biology · 2026Article
- Diabetic Atrial Cardiomyopathy: Pathogenesis, Diagnosis, Management, AI-Driven Diagnosis, and Risk Prediction.Journal of diabetes research · 2026Review
- 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
- Metabolic and Inflammatory Mechanisms Driving Atrial Fibrillation.Annual review of pharmacology and toxicology · 2026Review
- PFKFB2 Is Pivotal for Metabolic Flexibility and Differential Glucose Utilization.Journal of the American Heart Association · 2025Article
- Sensing within: Mitochondrial inside-out signal transduction.Cell chemical biology · 2025Review
- Concomitant Diabetes and Atrial Fibrillation: Epicardial Fat and Macrophage-Related Mechanisms.Diabetes/metabolism research and reviews · 2025Review
- Macrophage-mediated IL-6 signaling drives ryanodine receptor-2 calcium leak in postoperative atrial fibrillation.The Journal of clinical investigation · 2025Article
- Glucose metabolic dysregulation of diabetes and Its role in atrial fibrillation pathogenesis.Frontiers in cardiovascular medicine · 2025Review
- The ROS/CaMK II/β-Catenin Signaling Axis Affects the Osteogenic Potential of BMSCs and Disrupts Implant Osseointegration: An In Vitro Study.International journal of dentistry · 2025Article
- The treatment of myocardial ischemia-reperfusion injury: potential roles of natural drug modulating CaMKII.Frontiers in pharmacology · 2025Review
- The role of protein O-GlcNAcylation in diabetic cardiomyopathy.Biochemical Society transactions · 2024Review
Corrections and comments
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Authors and funding
22 authors at 5 institutions in 3 countries.
Funding
Abstract
Diabetes mellitus (DM) and atrial fibrillation (AF) are major unsolved public health problems, and diabetes is an independent risk factor for AF. However, the mechanism(s) underlying this clinical association is unknown. ROS and protein O-GlcNAcylation (OGN) are increased in diabetic hearts, and calmodulin kinase II (CaMKII) is a proarrhythmic signal that may be activated by ROS (oxidized CaMKII, ox-CaMKII) and OGN (OGN-CaMKII). We induced type 1 (T1D) and type 2 DM (T2D) in a portfolio of genetic mouse models capable of dissecting the role of ROS and OGN at CaMKII and global OGN in diabetic AF. Here, we showed that T1D and T2D significantly increased AF, and this increase required CaMKII and OGN. T1D and T2D both required ox-CaMKII to increase AF; however, we did not detect OGN-CaMKII or a role for OGN-CaMKII in diabetic AF. Collectively, our data affirm CaMKII as a critical proarrhythmic signal in diabetic AF and suggest ROS primarily promotes AF by ox-CaMKII, while OGN promotes AF by a CaMKII-independent mechanism(s). These results provide insights into the mechanisms for increased AF in DM and suggest potential benefits for future CaMKII and OGN targeted therapies.
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Registered trials
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.