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

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

In heart failure, increased CaMKII activity is decisively involved in arrhythmia formation. Here, the authors introduce the neuronal sodium channel NaV1.8 as a CaMKII downstream target as its specific knock-out reduces arrhythmias and improves survival in a CaMKII-overexpressing mouse model.

Bibliographic Details
Main Authors: Philipp Bengel, Nataliya Dybkova, Petros Tirilomis, Shakil Ahmad, Nico Hartmann, Belal A. Mohamed, Miriam Celine Krekeler, Wiebke Maurer, Steffen Pabel, Maximilian Trum, Julian Mustroph, Jan Gummert, Hendrik Milting, Stefan Wagner, Senka Ljubojevic-Holzer, Karl Toischer, Lars S. Maier, Gerd Hasenfuss, Katrin Streckfuss-Bömeke, Samuel Sossalla
Format: Article
Language:English
Published: Nature Portfolio 2021-11-01
Series:Nature Communications
Online Access:https://doi.org/10.1038/s41467-021-26690-1

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