Why the study?
Clinical use of doxorubicin is significantly limited by severe cardiotoxic effects, prompting investigation of underlying transcriptomic alterations.
Doxorubicin-induced cardiotoxicity in rats involves transcriptomic alterations affecting cardiac metabolism and circadian rhythm, providing potential targets for early biomarker discovery.
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Should not change doxorubicin care; leaves open whether circadian or cholesterol modulation mitigates cardiotoxicity in humans.
Doxorubicin is a member of the anthracycline class of chemotherapeutic agents and is among the most effective treatments available up to date. However, its clinical use is significantly limited by severe cardiotoxic effects. The purpose of this study is to investigate the transcriptomic alterations that occur in a rat model of doxorubicin-induced cardiotoxicity. Our results reveal significant dysregulations of cardiac metabolism and provide insights into the molecular mechanisms underlying cardiac damage produced by this treatment. Our analysis revealed that heart tissue recovery following doxorubicin treatment is hindered by hypercholesterolemia exacerbated by transcriptomic-level alteration of the circadian rhythm. This result could help facilitate the discovery of circulating biomarker-based early diagnostic methods for this disease, along with cardioprotective treatment implementation.
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Anca et al. (2025) studied this question.
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