• FGF13 deficiency mitigates doxorubicin-induced cardiotoxicity by improving cardiac function and reducing myocardial injury.
• Fgf13 knockout prevents DOX-induced cardiomyocyte apoptosis and mitochondrial damage.
• FGF13 interacts with Parkin, and its deficiency upregulates Parkin to confer cardioprotection.
• FGF13 represents a promising therapeutic target for preventing DOX-induced cardiotoxicity in cancer patients.