Papazoglou Panagiota, Peng Luying, Sachinidis Agapios
School of Pharmacy, Aristotle University of Thessaloniki, Thessaloniki, Greece.
Heart Health Center, Shanghai East Hospital, School of Medicine, Tongji University, Shanghai, China.
Front Cardiovasc Med. 2021 Apr 27;8:658900. doi: 10.3389/fcvm.2021.658900. eCollection 2021.
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."
抗癌药物的心血管毒性会促进心血管疾病的发展。因此，心血管毒性是一个重要的安全问题，在开发治疗癌症的药物和治疗应用时必须加以考虑。在抗癌药物中，蒽环类药物家族的成员，如阿霉素、柔红霉素和米托蒽醌，已知会导致心脏毒性甚至心力衰竭。利用人类诱导多能干细胞衍生的心肌细胞与“组学”技术相结合，我们确定了几种心脏毒性机制和信号转导途径。此外，这些药物通过多种机制，包括表观遗传机制，发挥心血管毒物的作用。在此，我们讨论主要的心血管毒性机制，重点关注与活性氧和线粒体相关的机制，这些机制会导致心脏毒性的表观遗传修饰。我们还讨论了如何使用现有的药物“武器”来减轻抗癌药物的心脏毒性作用。
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