Key result
This review details the specific intracellular activities of anthracyclines and highlights potential therapeutic windows for anthracycline-induced cardiomyopathy.
Why the study?
Despite the known risk of cardiotoxicity, anthracyclines remain widely prescribed, and no effective strategy has emerged to prevent cardiomyopathy, indicating a need for greater insight into underlying mechanisms.
This review summarizes the cellular and molecular mechanisms of anthracycline-induced cardiomyopathy to highlight potential therapeutic targets.
No effective anthracycline cardiomyopathy prevention has emerged beyond dexrazoxane; leaves open need for new mechanistic targets.
Despite the known risk of cardiotoxicity, anthracyclines are widely prescribed chemotherapeutic agents. They are broadly characterized as being a robust effector of cellular apoptosis in rapidly proliferating cells through its actions in the nucleus and formation of reactive oxygen species (ROS). And, despite the early use of dexrazoxane, no effective treatment strategy has emerged to prevent the development of cardiomyopathy, despite decades of study, suggesting that much more insight into the underlying mechanism of the development of cardiomyopathy is needed. In this review, we detail the specific intracellular activities of anthracyclines, from the cell membrane to the sarcoplasmic reticulum, and highlight potential therapeutic windows that represent the forefront of research into the underlying causes of anthracycline-induced cardiomyopathy.
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Dadson et al. (2020) conducted a review in Anthracycline-induced cardiomyopathy. Anthracyclines was evaluated. This review details the specific intracellular activities of anthracyclines and highlights potential therapeutic windows for anthracycline-induced cardiomyopathy.
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