Tirzepatide alleviates doxorubicin-induced cardiotoxicity via inhibiting HRD1-mediated Nrf2 ubiquitination

Our study suggested that TZP attenuated oxidative stress and cardiomyocyte apoptosis by modulating HRD1-mediated Nrf2 expression and activity, thereby protecting against the cardiotoxic effects exerted by DOX. These results supported that TZP might be a promising therapeutic option for reducing chemotherapy-related cardiotoxicity.