Targeting defective mitophagy offers potential therapeutic strategies to attenuate doxorubicin-induced cardiotoxicity, though clinical translation remains challenging.
Defective mitophagy is a key mechanism in doxorubicin-induced cardiotoxicity, presenting a potential but challenging therapeutic target for preventing heart failure in oncology patients.
Doxorubicin is a chemotherapeutic drug utilized for solid tumors and hematologic malignancies, but its clinical application is hampered by life-threatening cardiotoxicity, including cardiac dilation and heart failure. Mitophagy, a cargo-specific form of autophagy, is specifically used to eliminate damaged mitochondria in autophagosomes through hydrolytic degradation following fusion with lysosomes. Recent advances have unveiled a major role for defective mitophagy in the etiology of DOX-induced cardiotoxicity. Moreover, specific interventions targeting this mechanism to preserve mitochondrial function have emerged as potential therapeutic strategies to attenuate DOX-induced cardiotoxicity. However, clinical translation is challenging because of the unclear mechanisms of action and the potential for pharmacological adverse effects. This review aims to offer fresh perspectives on the role of mitophagy in the development of DOX-induced cardiotoxicity and investigate potential therapeutic strategies that focus on this mechanism to improve clinical management.
Zhang et al. (Tue,) conducted a review in Doxorubicin-Induced Cardiotoxicity. Mitophagy-targeted interventions was evaluated. Targeting defective mitophagy offers potential therapeutic strategies to attenuate doxorubicin-induced cardiotoxicity, though clinical translation remains challenging.