Why the study?
Despite extensive research, therapeutic options for anthracycline-induced cardiotoxicity remain limited, requiring detailed investigation to advance early diagnosis and cardioprotective strategies.
What are the pathogenetic mechanisms of cardiotoxicity associated with doxorubicin chemotherapy?
What are the pathogenetic mechanisms of cardiotoxicity associated with doxorubicin chemotherapy?
This review highlights that doxorubicin-induced cardiotoxicity is primarily driven by mitochondrial reactive oxygen species and oxidative stress, emphasizing the need for early diagnosis and cardioprotective therapy.
Emphasizes mitochondrial ROS targeting for cardioprotection in doxorubicin therapy; leaves open prospective validation in clinical trials.
Introduction . Long-term use of anthracyclines during cancer chemotherapy has been associated with the development of potentially life-threatening cardiotoxicity. Despite researches ongoing since the middle of the last century, approaches to the choice of therapy remain limited. Text . Doxorubicin currently is the most widely used chemotherapy. The leading side effect mechanism of the drug is the formation of reactive oxygen species in mitochondria with the mediated development of oxidative stress, which contributes to myocardial damage. However, despite the huge number of scientific papers devoted to various aspects of doxorubicin cardiotoxicity, its prevention and treatment, this issue requires detailed investigation in order to develop more advanced methods for early diagnosis and timely cardioprotective therapy. Conclusion . The current review discusses the pathogenetic mechanisms of cardiotoxicity associated with the use of doxorubicin chemotherapy. The pathogenesis of the cardiomyocytes death mechanism will provide an opportunity to develop new diagnostic and therapeutic approaches in the clinical practice.
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Andreev et al. (2024) studied this question.
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