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.
| Main Authors: | , , , , , , , , , , , , , , , , , , , |
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| Format: | Article |
| Language: | English |
| Published: |
Nature Portfolio
2021-11-01
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| Series: | Nature Communications |
| Online Access: | https://doi.org/10.1038/s41467-021-26690-1 |
| _version_ | 1818995804489121792 |
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| 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 |
| collection | DOAJ |
| 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. |
| first_indexed | 2024-12-20T21:19:40Z |
| format | Article |
| id | doaj.art-ba56cc69ae1140aebe506e2a3f9b30eb |
| institution | Directory Open Access Journal |
| issn | 2041-1723 |
| language | English |
| last_indexed | 2024-12-20T21:19:40Z |
| publishDate | 2021-11-01 |
| publisher | Nature Portfolio |
| record_format | Article |
| series | Nature Communications |
| spelling | doaj.art-ba56cc69ae1140aebe506e2a3f9b30eb2022-12-21T19:26:19ZengNature PortfolioNature Communications2041-17232021-11-0112111310.1038/s41467-021-26690-1Detrimental proarrhythmogenic interaction of Ca2+/calmodulin-dependent protein kinase II and NaV1.8 in heart failurePhilipp Bengel0Nataliya Dybkova1Petros Tirilomis2Shakil Ahmad3Nico Hartmann4Belal A. Mohamed5Miriam Celine Krekeler6Wiebke Maurer7Steffen Pabel8Maximilian Trum9Julian Mustroph10Jan Gummert11Hendrik Milting12Stefan Wagner13Senka Ljubojevic-Holzer14Karl Toischer15Lars S. Maier16Gerd Hasenfuss17Katrin Streckfuss-Bömeke18Samuel Sossalla19Clinic for Cardiology & Pneumology, Georg-August University GöttingenClinic for Cardiology & Pneumology, Georg-August University GöttingenClinic for Cardiology & Pneumology, Georg-August University GöttingenClinic for Cardiology & Pneumology, Georg-August University GöttingenClinic for Cardiology & Pneumology, Georg-August University GöttingenClinic for Cardiology & Pneumology, Georg-August University GöttingenClinic for Cardiology & Pneumology, Georg-August University GöttingenClinic for Cardiology & Pneumology, Georg-August University GöttingenClinic and Polyclinic for Internal Medicine II, University Medical Centre RegensburgClinic and Polyclinic for Internal Medicine II, University Medical Centre RegensburgClinic and Polyclinic for Internal Medicine II, University Medical Centre RegensburgHeart and Diabetes Centre North Rhine-WestphaliaHeart and Diabetes Centre North Rhine-WestphaliaClinic and Polyclinic for Internal Medicine II, University Medical Centre RegensburgDepartment of Cardiology, Medical University of GrazClinic for Cardiology & Pneumology, Georg-August University GöttingenClinic and Polyclinic for Internal Medicine II, University Medical Centre RegensburgClinic for Cardiology & Pneumology, Georg-August University GöttingenClinic for Cardiology & Pneumology, Georg-August University GöttingenClinic for Cardiology & Pneumology, Georg-August University GöttingenIn 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.https://doi.org/10.1038/s41467-021-26690-1 |
| spellingShingle | 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 Nature Communications |
| title | 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_short | 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 |
| url | https://doi.org/10.1038/s41467-021-26690-1 |
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