No abstract

Patients with cancer receiving doxorubicin-based chemotherapy often have to stop taking the drug due to its cardiotoxicity and therefore lose out on the beneficial effects of its potent antitumor activity. Doxorubicin has been demonstrated to damage cardiomyocytes via various mechanisms, including accumulation of reactive oxygen species (ROS), DNA damage and autophagy dysfunction. The present review focuses on autophagy, describing the general process of autophagy and the controversy surrounding its role in doxorubicin-induced cardiotoxicity. In addition, the associations between autophagy and apoptosis, ROS, DNA damage and inflammatory processes are discussed. In the future, it will be useful to further elucidate the process of autophagy and reveal its association with various pathological processes to develop effective strategies of preventing doxorubicin-induced cardiotoxicity.