| Article ID | Journal | Published Year | Pages | File Type |
|---|---|---|---|---|
| 8474607 | Journal of Molecular and Cellular Cardiology | 2014 | 12 Pages |
Abstract
Increased late INa (in disease-comparable ranges) induces proarrhythmogenic events during diastole in healthy and failing mouse myocytes, which are mediated via CaMKII-dependent SR Ca loss. Inhibition of late INa not only attenuated these cellular arrhythmias in mouse myocytes but also in failing human myocytes indicating some antiarrhythmic potential for an inhibition of the elevated late INa/CaMKII signaling pathway in this setting.
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Authors
Can M. Sag, Anika Mallwitz, Stefan Wagner, Nico Hartmann, Hanna Schotola, Thomas H. Fischer, Nele Ungeheuer, Jonas Herting, Ajay M. Shah, Lars S. Maier, Samuel Sossalla, Bernhard Unsöld,