ArticleCirculation. Arrhythmia and electrophysiology2009
Ca/calmodulin kinase II differentially modulates potassium currents.
Article in Circulation. Arrhythmia and electrophysiology, 2009. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 83 papers.
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Who cites it
83 citing papers in PubMed, 148 citations in OpenAlex.
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- Modeling autoregulation of cardiac excitation-Ca-contraction and arrhythmogenic activities in response to mechanical load changes.iScience · 2025Article
- Beta-Adrenergic Activation of the Inward Rectifier KInternational journal of molecular sciences · 2024Article
- The network of cardiac KNaunyn-Schmiedeberg's archives of pharmacology · 2024Review
- Computational Modeling of Cardiac Electrophysiology.Methods in molecular biology (Clifton, N.J.) · 2024Article
- Mechanisms of torsades de pointes: an update.Frontiers in cardiovascular medicine · 2024Review
- Integrative human atrial modelling unravels interactive protein kinase A and Ca2+/calmodulin-dependent protein kinase II signalling as key determinants of atrial arrhythmogenesis.Cardiovascular research · 2023Article
- KCells · 2023Review
- A Common East Asian aldehyde dehydrogenase 2*2 variant promotes ventricular arrhythmia with chronic light-to-moderate alcohol use in mice.Communications biology · 2023Article
- RBM24 controls cardiac QT interval through CaMKIIδ splicing.Cellular and molecular life sciences : CMLS · 2022Article
- Protein Kinase D1 Regulates Cardiac Hypertrophy, Potassium Channel Remodeling, and Arrhythmias in Heart Failure.Journal of the American Heart Association · 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
- Arrhythmogenic Remodeling in the Failing Heart.Cells · 2021Review
- Transcriptional profiles of genes related to electrophysiological function in Scn5aPhysiological reports · 2021Article
- Cellular Mechanisms of the Anti-Arrhythmic Effect of Cardiac PDE2 Overexpression.International journal of molecular sciences · 2021Article
- Stress-driven cardiac calcium mishandling via a kinase-to-kinase crosstalk.Pflugers Archiv : European journal of physiology · 2021Review
- Hyperglycemia regulates cardiac KBasic research in cardiology · 2020Article
- The oral Ca/calmodulin-dependent kinase II inhibitor RA608 improves contractile function and prevents arrhythmias in heart failure.ESC heart failure · 2020Article
- Functional modulation of sarcolemmal KAmerican journal of physiology. Cell physiology · 2020Article
23 more citing papers are in PubMed but not listed here.
Corrections and comments
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Authors and funding
11 authors at 1 institution in 1 country.
Funding
Abstract
backgroundPotassium currents contribute to action potential duration (APD) and arrhythmogenesis. In heart failure, Ca/calmodulin-dependent protein kinase II (CaMKII) is upregulated and can alter ion channel regulation and expression. METHODS AND
resultsWe examine the influence of overexpressing cytoplasmic CaMKIIdelta(C), both acutely in rabbit ventricular myocytes (24-hour adenoviral gene transfer) and chronically in CaMKIIdelta(C)-transgenic mice, on transient outward potassium current (I(to)), and inward rectifying current (I(K1)). Acute and chronic CaMKII overexpression increases I(to,slow) amplitude and expression of the underlying channel protein K(V)1.4. Chronic but not acute CaMKII overexpression causes downregulation of I(to,fast), as well as K(V)4.2 and KChIP2, suggesting that K(V)1.4 expression responds faster and oppositely to K(V)4.2 on CaMKII activation. These amplitude changes were not reversed by CaMKII inhibition, consistent with CaMKII-dependent regulation of channel expression and/or trafficking. CaMKII (acute and chronic) greatly accelerated recovery from inactivation for both I(to) components, but these effects were acutely reversed by AIP (CaMKII inhibitor), suggesting that CaMKII activity directly accelerates I(to) recovery. Expression levels of I(K1) and Kir2.1 mRNA were downregulated by CaMKII overexpression. CaMKII acutely increased I(K1), based on inhibition by AIP (in both models). CaMKII overexpression in mouse prolonged APD (consistent with reduced I(to,fast) and I(K1)), whereas CaMKII overexpression in rabbit shortened APD (consistent with enhanced I(K1) and I(to,slow) and faster I(to) recovery). Computational models allowed discrimination of contributions of different channel effects on APD.
conclusionsCaMKII has both acute regulatory effects and chronic expression level effects on I(to) and I(K1) with complex consequences on APD.
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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.