Table 1 Common anticancer therapies and their molecular mechanisms of cardiotoxicity
From: Precision cardio-oncology: understanding the cardiotoxicity of cancer therapy
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 |
