ArticleJournal of molecular and cellular cardiology plus2026
Persistently increased CaMKIIδ autophosphorylation mediates pathologic SR Ca loss in a murine model of Doxorubicin-induced cardiomyopathy.
Article in Journal of molecular and cellular cardiology plus, 2026. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 1 paper.
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The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
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Who cites it
1 citing paper in PubMed.
- Impact of CaInternational journal of molecular sciences · 2026Review
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9 authors.
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No grant is acknowledged in the PubMed record.
Abstract
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 pathologic Ca loss from the sarcoplasmic reticulum (SR). While CaMKIIδ is canonically activated by autophosphorylation, it can also be activated via oxidation. Objectives: We aimed to investigate the Methods: We utilized two transgenic mouse models, one lacking CaMKIIδ (CaMKIIδ Results: DOX Conclusions: Persistently increased CaMKIIδ autophosphorylation, but not oxidation, mediates pathologic SR Ca loss in Doxorubicin-induced cardiomyopathy.
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