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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| Автори: | , , , , , , , , , , , , , , , , , , , |
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| Формат: | Artigo |
| Мова: | Inglês |
| Опубліковано: |
Nature Portfolio
2021-11-01
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| Серія: | Nature Communications |
| Онлайн доступ: | https://doi.org/10.1038/s41467-021-26690-1 |
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