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Detrimental proarrhythmogenic interaction of Ca2+/calmodulin-dependent protein kinase II and NaV1.8 in heart failure

URN to cite this document:
urn:nbn:de:bvb:355-epub-520580
DOI to cite this document:
10.5283/epub.52058
Bengel, Philipp ; Dybkova, Nataliya ; Tirilomis, Petros ; Ahmad, Shakil ; Hartmann, Nico ; A. Mohamed, Belal ; Krekeler, Miriam Celine ; Maurer, Wiebke ; Pabel, Steffen ; Trum, Maximilian ; Mustroph, Julian ; Gummert, Jan ; Milting, Hendrik ; Wagner, Stefan ; Ljubojevic-Holzer, Senka ; Toischer, Karl ; Maier, Lars S. ; Hasenfuss, Gerd ; Streckfuss-Bömeke, Katrin ; Sossalla, Samuel
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Date of publication of this fulltext: 21 Apr 2022 14:49



Abstract

An interplay between Ca2+/calmodulin-dependent protein kinase IIδc (CaMKIIδc) and late Na+ current (INaL) is known to induce arrhythmias in the failing heart. Here, we elucidate the role of the sodium channel isoform NaV1.8 for CaMKIIδc-dependent proarrhythmia. In a CRISPR-Cas9-generated human iPSC-cardiomyocyte homozygous knock-out of NaV1.8, we demonstrate that NaV1.8 contributes to INaL ...

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