• Fgf13 deficiency mitigates doxorubicin-induced cardiotoxicity, improving cardiac function and reducing myocardial injury.
• Fgf13 knockout attenuates doxorubicin-induced cardiomyocyte apoptosis and mitochondrial damage.
• FGF13 interacts with Parkin, and its deficiency upregulates Parkin expression, suggesting a regulatory mechanism.
• FGF13 may serve as a promising therapeutic target for doxorubicin-induced cardiotoxicity.