Article

Inhibition of late INa prevents pathological hyperactivation of CaMKIIδ in a murine model of acute Doxorubicin-related cardiocellular toxicity

2026-01-02

Abstract excerpt

<h4>Background: </h4> and Purpose: Doxorubicin (DOX) represents a highly effective anthracycline, whose clinical application is limited by cardiotoxicity. The mechanisms underlying Doxorubicin-induced toxic cardiomyopathy (DICM) involve electrophysiological remodeling with intracellular Na overload as a consequence of increased late I Na , and hyperactivation of CaMKIIδ. Increased [Na] i contributes to CaMKIIδ a...

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Literature Corpus work: 9f26a8fa-6ccb-50d5-95d3-f944f3d232cb
DOI: 10.22541/au.176737886.69994326/v1

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