Anthracyclines are effective chemotherapeutic agents that are largely used in a number of malignancies. However, their use may be limited by severe adverse effects, including immunodepression and cardiotoxicity. Anthracyclines-induced cardiomyopathy is a serious and potentially lethal condition that fails to benefit from available therapies and may manifest both acutely and chronically, ultimately leading to heart failure. The incidence of cardiac side-effects is dose-dependent and may vary between 1.7% and 36%.

Scientists have worked for decades to define the etiopathogenesis of doxorubicin-induced cardiomyopathy and develop a strategy to achieve cardioprotection without reducing the antineoplastic activity of anthracyclines. It is highly probable that the toxicity for proliferating cells is based on a completely different mechanism compared to the one affecting cardiomyocytes. Many possible mechanisms have been proposed in past years and most were shown to be oxidative stress-based. However, ROS scavenging has proven to be insufficient to achieve cardioprotection, thus the molecular machinery triggered by ROS in anthracycline-induced cardiomyopathy is still being extensively dissected by the scientific community.

This Special Issue aims to serve as a resource for biomedical investigators at all levels, both those engaged in basic research as well as those involved in clinical practice to provide new insights that may help with future clinical translation of this area of research. Accordingly, we invite investigators to contribute original research and review articles that will help elucidate the molecular pathways underlining this complex iatrogenic condition. We encourage the submission of in vitro, ex vivo, in vivo, clinical studies and reviews describing the interplay between oxidative stress and inflammation, autophagy and cell death, the pathophysiological mechanisms underlying these associations and the modulatory roles of antioxidant and novel pharmaceutical compounds.

Potential topics include but are not limited to the following:

• Anthracyclines-triggered molecular pathways
• ROS scavenging in anthracycline-induced cardiomyopathy
• Crosstalk between ROS and inflammation in anthracycline-induced cardiomyopathy
• The role of mitochondrial dynamics and dysfunction in anthracycline side-effects
• Novel insight into the role of autophagy in anthracycline antineoplastic activity and side effects
• The direct and indirect role of anthracyclines in cell death
• Role and diagnostic potential of circulating ROS in anthracycline-induced cardiomyopathy
• Multi-organ cross-talk in anthracycline-induced cardiovascular dysfunction
• The role of anthracycline-induced ROS generation in models of cancer
• Cardiovascular toxicity in paediatric cancer survivors
• Personalized medicine in the prevention and treatment of anthracyclines cardiotoxicity