Recent Advances on Pathophysiology, Diagnostic and Therapeutic Insights in Cardiac Dysfunction Induced by Antineoplastic Drugs

Figure 1

Schematic representation of the main mechanisms by which cardiomyocytes are damaged by the most cardiotoxic anticancer agents among those currently in use. Anthracyclines induce a DNA damage response and reactive oxygen species (ROS) production; these two initial events result in a cascade of secondary alterations affecting mitochondrial integrity and function, intracellular calcium dynamics, and contractile proteins. By blocking the activity of tyrosine kinase receptors, such as vascular endothelial growth factor receptor (VEGFR) or ErbB2/ErbB4, bevacizumab, trastuzumab, and tyrosine kinase inhibitors (TKIs) alter mitochondria and modulate gene expression. SERCA2a: sarcoendoplasmic reticulum calcium ATPase. Black arrows indicate physiologic, homeostatic effects. Red arrows indicate deleterious effects. Modified from [5, 6].