Role of late sodium current as a potential arrhythmogenic mechanism in the progression of pressure-induced heart disease.
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Counteracting Protein Kinase Activity in the Heart: The Multiple Roles of Protein PhosphatasesCaMKII-dependent regulation of cardiac Na(+) homeostasisAberrant sodium influx causes cardiomyopathy and atrial fibrillation in miceVoltage-Gated Sodium Channel Phosphorylation at Ser571 Regulates Late Current, Arrhythmia, and Cardiac Function In Vivo.Toward a hierarchy of mechanisms in CaMKII-mediated arrhythmia.Ankyrin-G coordinates intercalated disc signaling platform to regulate cardiac excitability in vivoIntracellular Na+ overload causes oxidation of CaMKII and leads to Ca2+ mishandling in isolated ventricular myocytes.Effects of ranolazine on torsades de pointes tachycardias in a healthy isolated rabbit heart modelReduced immunoreactivities of B-type natriuretic peptide in pulmonary arterial hypertension rats after ranolazine treatmentCaMKII Phosphorylation of Na(V)1.5: Novel in Vitro Sites Identified by Mass Spectrometry and Reduced S516 Phosphorylation in Human Heart Failure.Misinterpretation of the mouse ECG: 'musing the waves of Mus musculus'.Role of CaMKII in cardiac arrhythmias.Inhibition of Late Sodium Current as an Innovative Antiarrhythmic Strategy.The Significance of the Late Na+ Current for Arrhythmia Induction and the Therapeutic Antiarrhythmic Potential of Ranolazine.Calmodulin/CaMKII inhibition improves intercellular communication and impulse propagation in the heart and is antiarrhythmic under conditions when fibrosis is absent.A novel computational model of mouse myocyte electrophysiology to assess the synergy between Na+ loading and CaMKII.C-terminal phosphorylation of NaV1.5 impairs FGF13-dependent regulation of channel inactivation.Sodium Channel Remodeling in Subcellular Microdomains of Murine Failing Cardiomyocytes.Reduction of SR Ca2+ leak and arrhythmogenic cellular correlates by SMP-114, a novel CaMKII inhibitor with oral bioavailability.Some 'brain' in the heart: a novel microdomain with neuronal Na channels responsible for arrhythmias?Ranolazine antagonizes catecholamine-induced dysfunction in isolated cardiomyocytes, but lacks long-term therapeutic effects in vivo in a mouse model of hypertrophic cardiomyopathy.Blockade of CaMKII depresses conduction preferentially in the right ventricular outflow tract and promotes ischemic ventricular fibrillation in the rabbit heart.Late sodium current dysregulation as a causal factor in arrhythmia.Myocyte [Na] Dysregulation in Heart Failure and Diabetic CardiomyopathyEmpagliflozin reduces Ca/calmodulin-dependent kinase II activity in isolated ventricular cardiomyocytes
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P2860
Role of late sodium current as a potential arrhythmogenic mechanism in the progression of pressure-induced heart disease.
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article científic
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article scientifique
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articolo scientifico
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artigo científico
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bilimsel makale
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scientific article published on 06 April 2013
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vedecký článok
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vetenskaplig artikel
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videnskabelig artikel
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vědecký článek
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name
Role of late sodium current as ...... ressure-induced heart disease.
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Role of late sodium current as ...... ressure-induced heart disease.
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Role of late sodium current as ...... ressure-induced heart disease.
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Role of late sodium current as ...... ressure-induced heart disease.
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Role of late sodium current as ...... ressure-induced heart disease.
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Role of late sodium current as ...... ressure-induced heart disease.
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P2093
P2860
P1476
Role of late sodium current as ...... ressure-induced heart disease.
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Bernhard C Danner
Jonas Herting
Karl Toischer
Lars S Maier
Luiz Belardinelli
Nico Hartmann
Peter J Mohler
Samuel Sossalla
Stefan Wagner
P2860
P304
P356
10.1016/J.YJMCC.2013.03.021
P577
2013-04-06T00:00:00Z