Epigenetic Mechanisms Involved in the Cardiovascular Toxicity of Anticancer Drugs

被引:12
作者
Papazoglou, Panagiota [1 ]
Peng, Luying [2 ,3 ]
Sachinidis, Agapios [4 ,5 ]
机构
[1] Aristotle Univ Thessaloniki, Sch Pharm, Thessaloniki, Greece
[2] Tongji Univ, Shanghai East Hosp, Sch Med, Heart Hlth Ctr, Shanghai, Peoples R China
[3] Tongji Univ, Inst Med Genet, Shanghai, Peoples R China
[4] Univ Cologne, Inst Neurophysiol, Fac Med, Cologne, Germany
[5] Univ Cologne, Ctr Mol Med Cologne, Cologne, Germany
来源
FRONTIERS IN CARDIOVASCULAR MEDICINE | 2021年 / 8卷
关键词
induced pluripotent stem cells; hiPSCs; cardiotoxicity; heart failure; genomics biomarkers; anthracyclines; anticancer therapy; epigenetic mechanisms; DOXORUBICIN-INDUCED CARDIOTOXICITY; DNA; MICRORNAS; METHYLATION; THERAPEUTICS; METABOLISM; SIGNATURES; CANCER; ROLES;
D O I
10.3389/fcvm.2021.658900
中图分类号
R5 [内科学];
学科分类号
1002 ; 100201 ;
摘要
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."
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页数:10
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