Nature Communications (Nov 2021)
Detrimental proarrhythmogenic interaction of Ca2+/calmodulin-dependent protein kinase II and NaV1.8 in heart failure
- 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
Affiliations
- Philipp Bengel
- Clinic for Cardiology & Pneumology, Georg-August University Göttingen
- Nataliya Dybkova
- Clinic for Cardiology & Pneumology, Georg-August University Göttingen
- Petros Tirilomis
- Clinic for Cardiology & Pneumology, Georg-August University Göttingen
- Shakil Ahmad
- Clinic for Cardiology & Pneumology, Georg-August University Göttingen
- Nico Hartmann
- Clinic for Cardiology & Pneumology, Georg-August University Göttingen
- Belal A. Mohamed
- Clinic for Cardiology & Pneumology, Georg-August University Göttingen
- Miriam Celine Krekeler
- Clinic for Cardiology & Pneumology, Georg-August University Göttingen
- Wiebke Maurer
- Clinic for Cardiology & Pneumology, Georg-August University Göttingen
- Steffen Pabel
- Clinic and Polyclinic for Internal Medicine II, University Medical Centre Regensburg
- Maximilian Trum
- Clinic and Polyclinic for Internal Medicine II, University Medical Centre Regensburg
- Julian Mustroph
- Clinic and Polyclinic for Internal Medicine II, University Medical Centre Regensburg
- Jan Gummert
- Heart and Diabetes Centre North Rhine-Westphalia
- Hendrik Milting
- Heart and Diabetes Centre North Rhine-Westphalia
- Stefan Wagner
- Clinic and Polyclinic for Internal Medicine II, University Medical Centre Regensburg
- Senka Ljubojevic-Holzer
- Department of Cardiology, Medical University of Graz
- Karl Toischer
- Clinic for Cardiology & Pneumology, Georg-August University Göttingen
- Lars S. Maier
- Clinic and Polyclinic for Internal Medicine II, University Medical Centre Regensburg
- Gerd Hasenfuss
- Clinic for Cardiology & Pneumology, Georg-August University Göttingen
- Katrin Streckfuss-Bömeke
- Clinic for Cardiology & Pneumology, Georg-August University Göttingen
- Samuel Sossalla
- Clinic for Cardiology & Pneumology, Georg-August University Göttingen
- DOI
- https://doi.org/10.1038/s41467-021-26690-1
- Journal volume & issue
-
Vol. 12,
no. 1
pp. 1 – 13
Abstract
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.
