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ABSTRACT: Background
Cardiotoxicity of doxorubicin, a chemotherapy medication, remains the most dangerous side effect. CISD2 plays a critical role during cardiac aging.Objectives
We use a potent CISD2 activator, hesperetin, to ameliorate doxorubicin-induced cardiotoxicity by upregulating CISD2 in mice.Methods
Two animal models, an acute and a tumor-bearing doxorubicin-induced cardiotoxicity model, were used in this study. Both genetic and pharmacological approaches were employed. Transgenic mice and a potent CISD2 activator, hesperetin, were utilized to ameliorate doxorubicin-induced cardiotoxicity by upregulating CISD2 expression in mice. Additionally, a human-derived iPSC system was used to provide human-relevant evidence. Comprehensive biological, histological, transcripto
SUBMITTER: Chou YJ
PROVIDER: S-EPMC12409322 | biostudies-literature | 2025 Aug
REPOSITORIES: biostudies-literature