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Persistently increased CaMKIIδ autophosphorylation mediates pathologic SR Ca loss in a murine model of Doxorubicin-induced cardiomyopathy

Background: Doxorubicin (DOX)-induced cardiomyopathy (DICM) manifests as left ventricular (LV) systolic dysfunction. DOX triggers oxidative stress and CaMKIIδ activity in cardiac myocytes. CaMKIIδ activation leads to impaired intracellular Ca handling and contractile dysfunction because of pathologi...

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Bibliografiske detaljer
Principais autores: Anna-Lena Feder, Daniel Tarnowski, Anna-Maria Pfützenreuter, Maria Johanna Baier, Julian Mustroph, Maithily S. Nanadikar, Dörthe M. Katschinski, Lars Siegfried Maier, Can Martin Sag
Format: Artigo
Sprog:Inglês
Udgivet: Elsevier 2026-03-01
Serier:Journal of Molecular and Cellular Cardiology Plus
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Online adgang:http://www.sciencedirect.com/science/article/pii/S2772976125005471
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