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Author

Weiping Du

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Sep 2026

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...

Jian Wang, Jie Zhang, Nan Wu et al. · 0 citations

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