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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| Principais autores: | , , , , , , , , |
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| Format: | Artigo |
| Sprog: | Inglês |
| Udgivet: |
Elsevier
2026-03-01
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| Serier: | Journal of Molecular and Cellular Cardiology Plus |
| Fag: | |
| Online adgang: | http://www.sciencedirect.com/science/article/pii/S2772976125005471 |
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