Diastolic dysfunction and arrhythmias caused by overexpression of CaMKIIδ(C) can be reversed by inhibition of late Na(+) current

Transgenic (TG) Ca(2+)/calmodulin-dependent protein kinase II (CaMKII) δ(C) mice develop systolic heart failure (HF). CaMKII regulates intracellular Ca(2+) handling proteins as well as sarcolemmal Na(+) channels. We hypothesized that CaMKII also contributes to diastolic dysfunction and arrhythmias v...

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Detalles Bibliográficos
Autores principales: Sossalla, Samuel, Maurer, Ulrike, Schotola, Hanna, Hartmann, Nico, Didié, Michael, Zimmermann, Wolfram-H., Jacobshagen, Claudius, Wagner, Stefan, Maier, Lars S.
Formato: Texto
Lenguaje:English
Publicado: Springer-Verlag 2010
Materias:
Original Contribution
Acceso en línea:https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3032905/
https://www.ncbi.nlm.nih.gov/pubmed/21174213
http://dx.doi.org/10.1007/s00395-010-0136-x

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