Doxorubicin-Induced Cardiotoxicity: Mechanisms and Management

Abstract

Unfortunately, anticancer medications are extremely harmful to normal cells. Doxorubicin (DOX) is a highly cardiotoxic medication that can result in cardiomyopathy. The most significant mechanism for DOX-induced cardiotoxicity is oxidative stress, while other pathways have also been put forth. This review aims to highlight the mechanisms of DOX-induced cardiotoxicity and the most updated managements. Trustworthy sites such as Google Scholar, PubMed, and Research Gate were used to find the most updated articles. Many titles have been used for searching, such as "doxorubicin and cardiotoxicity," "cardioprotection," and "cardio-protective effects of phytochemicals." Preprints, review articles, and research with meta-analyses were disregarded. Three pathways, including oxidative stress, mitochondrial damage, and calcium excess, were responsible for DOX-induced cardiotoxicity. Cardiotoxicity may be partially caused by cell death, activation of the ubiquitin-ligase-proteasome system, and changes in its gene expression brought on by DOX. In the instance of DOX cardiotoxicity, medications and nutraceuticals with antioxidants and iron chelating properties have been found to have cardio-protective benefits. In conclusion, doxorubicin-treated cancer patients have been linked to cardiotoxicity, making cardioprotection extremely important in these patients. All of the mechanisms included in this review's discussion might provide light on fresh approaches to the treatment and/or prevention of DOX-induced cardiotoxicity.