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