Table 1.
Common anticancer therapies and their molecular mechanisms of cardiotoxicity
| Anticancer therapies | Molecular mechanisms of cardiotoxicity |
|---|---|
| Anthacyclines | Activate Necleus TopIIβ (inhibited by Dexrazoxane) |
| Generate ROS | |
| Activate TopImt | |
| Fe2+ overload (chealated by Dexrazoxane) | |
| Damage transcription | |
| Energy depletion | |
| Prevent DNA repair | |
| Alkylating agents | Cause endothelial dysfunction |
| Cause thrombosis | |
| Direct DNA damage | |
| HER2/ERB2 Ab | Inhibit Pro-Survival NRG-1/ErbB Pathway |
| Generate ROS | |
| TKIs/VEGFR Ab | Inhibit angiogenesis |
| Cause endothelial dysfunction | |
| Cause energy depletion | |
| Antimetabolites | Inhibit angiogenesis |
| Cause endothelial dysfunction | |
| Cause energy depletion | |
| Generate ROS | |
| Antimicrotubules | Inhibit microtubule formation |
| Activate NCS-1 causing Ca2+ overload | |
| Radiation therapy | Inhibit angiogenesis |
| Cause endothelial dysfunction | |
| Cause energy depletion | |
| Generate ROS |
TKIs tyrosine kinase inhibitors, VEGFR vascular endothelial growth factor receptor, NRG-1 neuregulin-1, HER2/ErbB2 human epidermal growth factor receptor 2, Ab antibody, TopImt mitochondrial topoisomerase I, TopIIβ topoisomerase IIβ, ROS reactive oxygen species, NCS-1 neuronal calcium sensor 1