| Article ID | Journal | Published Year | Pages | File Type |
|---|---|---|---|---|
| 5959846 | Heart Rhythm | 2015 | 12 Pages |
Abstract
Our data suggest that CaMKII inhibition is effective in preventing arrhythmogenesis in the setting of junctin ablation through modulation of both SR Ca2+ release and uptake. Thus, it merits further investigation as promising molecular therapy.
Keywords
SOICRCPVTPLNRyRCSQpKaCaMKIIDADJunctinSVTSCDsarco-endoplasmic reticulum calcium ATPaseArrhythmiaElectrocardiographyECGPremature ventricular contractionisoproterenolVentricular tachycardiaBidirectional ventricular tachycardiaSustained ventricular tachycardiaCatecholaminergic polymorphic ventricular tachycardiaSarcoplasmic reticulumphospholambanSERCASudden cardiac deathwild-typeprotein kinase Acalcium/calmodulin-dependent protein kinase IIdelayed afterdepolarizationPVCCalsequestrinRyanodine receptor
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Authors
Christos PhD, John MD, Stephan E. MD, Evangelia G. PhD, Despina PhD, FACMG,