Improvements in screening strategies and novel anti-tumor drugs promote longer survival of cancer patients, but many drugs also have serious side effects including both short-term and long-term cardiotoxicity. Oxidative stress (OS) is the major effect of anti-tumor drug-induced cardiotoxicity and is caused by an imbalance between reactive oxygen species (ROS) and endogenous antioxidants in response to injury, leading to myocardial toxicity.

Though the role of oxidative stress in anti-tumor drug-induced cardiotoxicity has been identified, prevention strategies have been far from successful. Many studies describe anti-tumor drug therapy for cardiotoxicity, including dexrazoxane, natural plant extracts, animal extracts, or chemically synthesized artificial antioxidants. The success of animal modeling in various drug efficacy studies does not translate to good results in humans, and, even if it did, large-scale clinical trials are lacking.

This Special Issue aims to summarize the present knowledge of oxidative stress in anti-tumor drug-induced cardiotoxicity including cell molecular mechanisms, prevention and treatment strategies, drug research, and population experiments. Original research and review articles are welcome.

Potential topics include but are not limited to the following:

• The prevention of oxidative stress induced by anti-tumor drugs
• Subcellular organelle damage in anti-tumor drug-induced oxidative stress
• Dysregulation of protein regulation in anti-tumor drug-induced oxidative stress
• Role of nitric oxide synthase in anti-tumor drug-induced cardiotoxicity
• Role of NADPH oxidase in anti-tumor drug-induced cardiotoxicity