Key result
Major anti-cancer drugs frequently cause cardiotoxicity driven by oxidative stress, autophagy, apoptosis, and inflammation.
Why the study?
Increasing effectiveness of chemotherapeutic drugs has been associated with growing cardiovascular adverse effects that in many cases are more significant than the underlying disease.
This review summarizes the pathophysiological mechanisms of cardiotoxicity for major classes of chemotherapeutic agents, highlighting the importance of cardio-oncology.
Certain success has been achieved in the treatment of cancer due to the development of various effective chemotherapeutic drugs. However, an increase in their effectiveness (aggressiveness) was associated with a growth of undesirable effects on the entire human body, in particular, on the cardiovascular system. The damage to the cardiovascular system from chemotherapy in many cases is more significant than from the underlying disease. In recent years, a new direction of medicine has been formed - cardio-oncology. The major groups of cardiotoxic chemotherapeutic agents are anthracyclines, inhibitors of epidermal growth factor receptor type 2 (anti-HER2), antimetabolites, microtubule inhibitors, proteasome inhibitors, platinum-based chemotherapeutic drugs, and angiogenesis inhibitors (inhibitors of vascular endothelial growth factor). This review discusses principal pathophysiological mechanisms of the cardiotoxicity of these chemotherapeutic drugs.
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Chaulin et al. (2020) conducted a review in Chemotherapy-induced cardiotoxicity. Chemotherapeutic agents was evaluated. Cardiotoxicity is a common adverse consequence of major anti-cancer drugs, driven by multiple pathophysiological mechanisms including oxidative stress, autophagy, apoptosis, and inflammation.
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