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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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書誌詳細
主要な著者: 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
フォーマット: Artigo
言語:Inglês
出版事項: Elsevier 2026-03-01
シリーズ:Journal of Molecular and Cellular Cardiology Plus
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オンライン・アクセス:http://www.sciencedirect.com/science/article/pii/S2772976125005471
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