Article
Diastolic dysfunction and arrhythmias caused by overexpression of CaMKIIδ(C) can be reversed by inhibition of late Na(+) current.
Basic research in cardiology - 1 Mar 2011
Sossalla Samuel, Maurer Ulrike, Schotola Hanna, Hartmann Nico, Didié Michael, Zimmermann Wolfram-H, Jacobshagen Claudius, Wagner Stefan, Maier Lars S
Abstract excerpt
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 via augmentation of the late Na(+) current (late I(Na)) in early HF (8-week-old TG mice). Echocardiography revealed...
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