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Updated: Nov 5, 2025

Chemotherapy-induced Vascular Toxicity - Real-time In vivo Imaging of Vessel Impairment
Published on: January 7, 2015
Epigenetic Mechanisms Involved in the Cardiovascular Toxicity of Anticancer Drugs
Panagiota Papazoglou1, Luying Peng2,3, Agapios Sachinidis4,5
1School of Pharmacy, Aristotle University of Thessaloniki, Thessaloniki, Greece.
Abstract:
The cardiovascular toxicity of anticancer drugs promotes the development of cardiovascular diseases. Therefore, cardiovascular toxicity is an important safety issue that must be considered when developing medications and therapeutic applications to treat cancer. Among anticancer drugs, members of the anthracycline family, such as doxorubicin, daunorubicin and mitoxantrone, are known to cause cardiotoxicity and even heart failure. Using human-induced pluripotent stem cell-derived cardiomyocytes in combination with "Omic" technologies, we identified several cardiotoxicity mechanisms and signal transduction pathways. Moreover, these drugs acted as cardiovascular toxicants through a syndrome of mechanisms, including epigenetic ones. Herein, we discuss the main cardiovascular toxicity mechanisms, with an emphasis on those associated with reactive oxygen species and mitochondria that contribute to cardiotoxic epigenetic modifications. We also discuss how to mitigate the cardiotoxic effects of anticancer drugs using available pharmaceutical "weapons."
Insights
Anticancer drugs like anthracyclines can cause heart failure. This study identifies cardiotoxicity mechanisms, including epigenetic changes, and discusses mitigation strategies for safer cancer treatment.
Area of Science:
- Cardiology
- Oncology
- Toxicology
- Epigenetics
Background:
- Cardiovascular toxicity is a significant concern with anticancer drugs, potentially leading to heart failure.
- Anthracyclines (doxorubicin, daunorubicin, mitoxantrone) are known for their cardiotoxic effects.
Purpose of the Study:
- To identify cardiotoxicity mechanisms induced by anticancer drugs.
- To explore the role of epigenetic modifications in drug-induced cardiotoxicity.
- To discuss strategies for mitigating anticancer drug cardiotoxicity.
Main Methods:
- Utilized human-induced pluripotent stem cell-derived cardiomyocytes.
- Employed "Omic" technologies for pathway and mechanism identification.
- Focused on reactive oxygen species and mitochondrial pathways.
Main Results:
- Identified multiple mechanisms and signal transduction pathways contributing to cardiotoxicity.
- Demonstrated that anticancer drugs induce cardiovascular toxicity via epigenetic mechanisms.
- Highlighted the role of reactive oxygen species and mitochondria in cardiotoxic epigenetic modifications.
Conclusions:
- Anticancer drug cardiotoxicity involves complex mechanisms, including epigenetic alterations.
- Understanding these mechanisms is crucial for developing safer cancer therapies.
- Pharmaceutical interventions can potentially mitigate the cardiotoxic effects of these drugs.
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