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OPENCitation: Cell Death and Illness (2013) four, e843; doi:ten.1038/cddis.2013.369 2013 Macmillan Publishers Limited All rights reserved 2041-4889/nature/cddisCaMKII inhibition rectifies arrhythmic phenotype in a patient-specific model of catecholaminergic polymorphic ventricular tachycardiaE Di Pasquale1,9,10, F Lodola2,9, M Miragoli3,4, M Denegri2, JE Avelino-Cruz2,11, M Buonocore5, H Nakahama3, P Portararo6, R Bloise2, C Napolitano2,7, G Condorelli,4 and SG Priori,two,7,Induced pluripotent stem cells (iPSC) give a unique opportunity for developmental research, illness modeling and regenerative medicine approaches in humans. The aim of our study was to create an in vitro `patient-specific cell-based system’ that could facilitate the screening of new therapeutic molecules for the treatment of catecholaminergic polymorphic ventricular tachycardia (CPVT), an inherited form of fatal arrhythmia. Right here, we report the development of a cardiac model of CPVT by way of the generation of iPSC from a CPVT patient carrying a heterozygous mutation within the cardiac ryanodine receptor gene (RyR2) and their subsequent differentiation into cardiomyocytes (CMs). Whole-cell patch-clamp and intracellular electrical recordings of spontaneously beating cells revealed the presence of delayed afterdepolarizations (DADs) in CPVT-CMs, both in resting PDE2 Inhibitor Compound conditions and just after b-adrenergic stimulation, resembling the cardiac phenotype from the patients. Additionally, treatment with KN-93 (2-[N-(2-hydroxyethyl)]-N-(4methoxybenzenesulfonyl)]amino-N-(4-chlorocinnamyl)-N-methylbenzylamine), an antiarrhythmic drug that inhibits Ca2 ?/calmodulin-dependent serine hreonine protein kinase II (CaMKII), drastically decreased the presence of DADs in CVPT-CMs, rescuing the arrhythmic phenotype induced by catecholamine.