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.

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Autores principales: 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
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Lenguaje:EN
Publicado: Nature Portfolio 2021
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Acceso en línea:https://doaj.org/article/ba56cc69ae1140aebe506e2a3f9b30eb
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spelling oai:doaj.org-article:ba56cc69ae1140aebe506e2a3f9b30eb2021-11-21T12:34:22ZDetrimental proarrhythmogenic interaction of Ca2+/calmodulin-dependent protein kinase II and NaV1.8 in heart failure10.1038/s41467-021-26690-12041-1723https://doaj.org/article/ba56cc69ae1140aebe506e2a3f9b30eb2021-11-01T00:00:00Zhttps://doi.org/10.1038/s41467-021-26690-1https://doaj.org/toc/2041-1723In 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.Philipp BengelNataliya DybkovaPetros TirilomisShakil AhmadNico HartmannBelal A. MohamedMiriam Celine KrekelerWiebke MaurerSteffen PabelMaximilian TrumJulian MustrophJan GummertHendrik MiltingStefan WagnerSenka Ljubojevic-HolzerKarl ToischerLars S. MaierGerd HasenfussKatrin Streckfuss-BömekeSamuel SossallaNature PortfolioarticleScienceQENNature Communications, Vol 12, Iss 1, Pp 1-13 (2021)
institution DOAJ
collection DOAJ
language EN
topic Science
Q
spellingShingle Science
Q
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
Detrimental proarrhythmogenic interaction of Ca2+/calmodulin-dependent protein kinase II and NaV1.8 in heart failure
description 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.
format article
author 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
author_facet 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
author_sort Philipp Bengel
title Detrimental proarrhythmogenic interaction of Ca2+/calmodulin-dependent protein kinase II and NaV1.8 in heart failure
title_short Detrimental proarrhythmogenic interaction of Ca2+/calmodulin-dependent protein kinase II and NaV1.8 in heart failure
title_full Detrimental proarrhythmogenic interaction of Ca2+/calmodulin-dependent protein kinase II and NaV1.8 in heart failure
title_fullStr Detrimental proarrhythmogenic interaction of Ca2+/calmodulin-dependent protein kinase II and NaV1.8 in heart failure
title_full_unstemmed Detrimental proarrhythmogenic interaction of Ca2+/calmodulin-dependent protein kinase II and NaV1.8 in heart failure
title_sort detrimental proarrhythmogenic interaction of ca2+/calmodulin-dependent protein kinase ii and nav1.8 in heart failure
publisher Nature Portfolio
publishDate 2021
url https://doaj.org/article/ba56cc69ae1140aebe506e2a3f9b30eb
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