ArticleCirculation2002
Calmodulin kinase II and arrhythmias in a mouse model of cardiac hypertrophy.
Article in Circulation, 2002. The graph could read no effect estimate from its abstract, so it casts no vote on the map. It has been retracted, and should not be counted. Cited by 112 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
112 citing papers in PubMed, 264 citations in OpenAlex.
- Role of CAMK2D in neurodevelopment and associated conditions.American journal of human genetics · 2024Article
- Histone deacetylase functions and therapeutic implications for adult skeletal muscle metabolism.Frontiers in molecular biosciences · 2023Review
- Calcium Signalling in Heart and Vessels: Role of Calmodulin and Downstream Calmodulin-Dependent Protein Kinases.International journal of molecular sciences · 2022Review
- Sodium dichloroacetate stimulates cardiac mitochondrial metabolism and improves cardiac conduction in the ovine fetus during labor.American journal of physiology. Regulatory, integrative and comparative physiology · 2022Article
- The Oxidative Balance Orchestrates the Main Keystones of the Functional Activity of Cardiomyocytes.Oxidative medicine and cellular longevity · 2022Review
- Late sodium current and calcium homeostasis in arrhythmogenesis.Channels (Austin, Tex.) · 2021Review
- Moving average and standard deviation thresholding (MAST): a novel algorithm for accurate R-wave detection in the murine electrocardiogram.Journal of comparative physiology. B, Biochemical, systemic, and environmental physiology · 2021Article
- Loss of CASK Accelerates Heart Failure Development.Circulation research · 2021Article
- Melatonin to Rescue the Aged Heart: Antiarrhythmic and Antioxidant Benefits.Oxidative medicine and cellular longevity · 2021Review
- Mitochondrial CaMKII causes adverse metabolic reprogramming and dilated cardiomyopathy.Nature communications · 2020Article
- Regulation of cardiovascular calcium channel activity by post-translational modifications or interacting proteins.Pflugers Archiv : European journal of physiology · 2020Review
- A compartmentalized mathematical model of mouse atrial myocytes.American journal of physiology. Heart and circulatory physiology · 2020Article
- Role of Oxidation-Dependent CaMKII Activation in the Genesis of Abnormal Action Potentials in Atrial Cardiomyocytes: A Simulation Study.BioMed research international · 2020Article
- Challenges and Opportunities for Therapeutic Targeting of Calmodulin Kinase II in Heart.Frontiers in pharmacology · 2020Review
- Programmed necrosis in cardiomyocytes: mitochondria, death receptors and beyond.British journal of pharmacology · 2019Review
- CaMKII-dependent late NaAmerican journal of physiology. Heart and circulatory physiology · 2018Article
- Antioxidant defense and protection against cardiac arrhythmias: lessons from a mammalian hibernator (the woodchuck).FASEB journal : official publication of the Federation of American Societies for Experimental Biology · 2018Article
- CaMKII inhibition reduces isoproterenol-induced ischemia and arrhythmias in hypertrophic mice.Oncotarget · 2017Article
- CaMKII is a nodal signal for multiple programmed cell death pathways in heart.Journal of molecular and cellular cardiology · 2017Review
- Species-Dependent Mechanisms of Cardiac Arrhythmia: A Cellular Focus.Clinical Medicine Insights. Cardiology · 2017Review
52 more citing papers are in PubMed but not listed here.
Corrections and comments
- Expression of concern · 2015-02-17Falsification/Fabrication of Data · Falsification/Fabrication of Image · Investigation by Company/Institution · Investigation by ORI · Misconduct - Official Investigation(s) and/or Finding(s) · Misconduct by Author · Unreliable Data · · I Dzhura named for misconduct; See also Findings of Research Misconduct: https://www.ncbi.nlm.nih.gov/pmc/articles/PMC5019549/;
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Authors and funding
11 authors at 1 institution in 1 country.
Funding
Abstract
backgroundCalmodulin kinase (CaMK) II is linked to arrhythmia mechanisms in cellular models where repolarization is prolonged. CaMKII upregulation and prolonged repolarization are general features of cardiomyopathy, but the role of CaMKII in arrhythmias in cardiomyopathy is unknown. METHODS AND
resultsWe studied a mouse model of cardiac hypertrophy attributable to transgenic (TG) overexpression of a constitutively active form of CaMKIV that also has increased endogenous CaMKII activity. ECG-telemetered TG mice had significantly more arrhythmias than wild-type (WT) littermate controls at baseline, and arrhythmias were additionally increased by isoproterenol. Arrhythmias were significantly suppressed by an inhibitory agent targeting endogenous CaMKII. TG mice had longer QT intervals and action potential durations than WT mice, and TG cardiomyocytes had frequent early afterdepolarizations (EADs), a hypothesized mechanism for triggering arrhythmias. EADs were absent in WT cells before and after isoproterenol, whereas EAD frequency was unaffected by isoproterenol in TG mice. L-type Ca2+ channels (LTTCs) can activate EADs, and LTCC opening probability (Po) was significantly higher in TG than WT cardiomyocytes before and after isoproterenol. A CaMKII inhibitory peptide equalized TG and WT LTCC Po and eliminated EADs, whereas a peptide antagonist of the Na+/Ca2+ exchanger current, also hypothesized to support EADs, was ineffective.
conclusionsThese findings support the hypothesis that CaMKII is a proarrhythmic signaling molecule in cardiac hypertrophy in vivo. Cellular studies point to EADs as a triggering mechanism for arrhythmias but suggest that the increase in arrhythmias after beta-adrenergic stimulation is independent of enhanced EAD frequency.
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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.