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. 2021 Apr 12;11:7954. doi: 10.1038/s41598-021-87209-8

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© The Author(s) 2021

Open Access This article is licensed under a Creative Commons Attribution 4.0 International License, which permits use, sharing, adaptation, distribution and reproduction in any medium or format, as long as you give appropriate credit to the original author(s) and the source, provide a link to the Creative Commons licence, and indicate if changes were made. The images or other third party material in this article are included in the article's Creative Commons licence, unless indicated otherwise in a credit line to the material. If material is not included in the article's Creative Commons licence and your intended use is not permitted by statutory regulation or exceeds the permitted use, you will need to obtain permission directly from the copyright holder. To view a copy of this licence, visit http://creativecommons.org/licenses/by/4.0/.

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Schematic representation of anthracyclines induced cardiotoxicity. The treatment of breast cancer patients with an anthracycline regimen results in excessive ROS production with subsequent oxidant stress and inflammation in the cardiomyocyte. Anthracycline treatment also results in double strand DNA damage as well as cellular apoptosis which further contributes to the cardiotoxicity. The upregulation of biomarkers and circulating miRNAs associated with these pathological mechanisms operant in response to anthracycline treatment contributes to a decline in LVEF and altered cardiomyocytes, hence predicting early cardiotoxicity events.