Anthracycline cardiotoxicity remains a serious problem in pediatric and adult cancer survivors. This chapter discusses the involvement of multiple cardiac cell types in the pathogenesis of the onset and progression of doxorubicin cardiotoxicity. In addition to cardiomyocytes, considered the classical cellular target, the role of cardiac fibroblasts and vascular cells together with progenitor cells of cardiac and extra-cardiac origin is addressed with a focus on oxidative stress, DNA damage, senescence, cell death, and molecular signals involved in cellular injury and response. Current strategies for primary and secondary prevention aiming at contrasting the onset of early and late doxorubicin-induced toxic events do not completely resolve the growing clinical problem. Thus, there is the necessity to understand cellular processes that operate within and beyond cardiomyocyte, to develop more effective tools for the prevention and treatment of progressive cardiomyopathy in otherwise successfully treated oncologic patients.
Part of the book: Cardiotoxicity