CTRP4 overexpression mitigates doxorubicin-induced cardiotoxicity by suppressing oxidative stress and ferroptosis through activation of the Sirt1-Nrf2 signaling axis.
Oxidative stress and ferroptosis are major drivers of doxorubicin (DOX)-induced cardiotoxicity. C1q/TNF-related protein 4 (CTRP4) is an endogenous cardioprotective factor that modulates both processes; however, its role and underlying mechanisms in DOX-induced myocardial injury remain unclear. We hypothesized that CTRP...