Oxidative stress-mediated signaling acts as a critical modulator in anthracycline-induced cardiotoxicity, suggesting that interventions modulating redox balance may serve as primary prevention.
This review highlights the reemerging importance of oxidative stress in anthracycline-induced cardiotoxicity and suggests that preventive therapies may work through modulating redox balance.
Anthracycline‐induced cardiotoxicity (AIC) persists as a significant cause of morbidity and mortality in cancer survivors. Although many protective strategies have been evaluated, cardiotoxicity remains an ongoing threat. The mechanisms of AIC remain unclear; however, several pathways have been proposed, suggesting a multifactorial origin. When the central role of topoisomerase 2 β in the pathophysiology of AIC was described some years ago, the classical reactive oxygen species (ROS) hypothesis shifted to a secondary position. However, new insights have reemphasized the importance of the role of oxidative stress‐mediated signaling as a common pathway and a critical modulator of the different mechanisms involved in AIC. A better understanding of the mechanisms of cardiotoxicity is crucial for the development of treatment strategies. It has been suggested that the available therapeutic interventions for AIC could act on the modulation of oxidative balance, leading to a reduction in oxidative stress injury. These indirect antioxidant effects make them an option for the primary prevention of AIC. In this review, our objective is to provide an update of the accumulated knowledge on the role of oxidative stress in AIC and the modulation of the redox balance by potential preventive strategies.
Carrasco et al. (Fri,) conducted a review in Anthracycline-induced cardiotoxicity. Preventive strategies modulating redox balance was evaluated. Oxidative stress-mediated signaling acts as a critical modulator in anthracycline-induced cardiotoxicity, suggesting that interventions modulating redox balance may serve as primary prevention.