MicroRNAs in Cancer Treatment-Induced Cardiotoxicity

Figures

• 

  Figure 1. Mechanisms of cardiotoxicity induced by different classes of anticancer therapies. Treatment for cancer diseases can adversely affect both the heart and the vasculature, leading to death of cardiomyocytes, endothelial dysfunction, and, consequently, different cardiovascular complications. Common cellular targets and pathways involved in cardiotoxicity linked to anthracyclines (A), ErbB2 inhibitors (B), VEGF inhibitors (C), anti-BCR-Abl agents (D), radiation therapy and immunotherapy (in particular checkpoint inhibitors) (E), and other commonly used, less specific antineoplastic drugs (antimetabolites, proteasome inhibitors, and taxanes) (F) are schematically illustrated. Abbreviations: ANTs, anthracyclines; TopIIβ, topoisomerase IIβ; ROS, reactive oxygen species; RNS, reactive nitrogen species; LV, left ventricular; RV, right ventricular; HF, heart failure; ErbB2/ErbB4, human epidermal growth factor receptor 2/4; VEGF, vascular endothelial growth factor; R, receptor; TKs, tyrosine kinases; TKIs, tyrosine kinase inhibitors; ER, endoplasmic reticulum; PAD, peripheral artery disease; PD-1, programmed cell death protein 1; PD-L1, programmed cell death protein ligand 1.