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Visnagin is highlighted as a potential protectant against doxorubicin-induced cardiotoxicity, which is primarily driven by oxidative stress and altered mitochondrial energetics.
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Discusses the mechanisms of doxorubicin-induced cardiotoxicity and the potential role of visnagin as a cardioprotectant.
Doxorubicin (DOX) is a broad-spectrum and potent anthracycline antibiotic that has been widely used since 1960s as a chemotherapeutic agent to treat a variety of human cancers (1). Despite its superior anti-cancer efficacy, the clinical use of DOX is often limited by dose-dependent cardiotoxicity, which may lead to irreversible dilated cardiomyopathy and congestive heart failure (2,3). Currently predominant theories for explaining DOX cardiotoxicity include the DOX-induced increase of oxidative stress in cardiomyocytes (4), alteration of mitochondrial energetics (5,6), and direct effect on DNA. Particularly, anthracyclines promote the formation of reactive oxygen species (ROS) through redox cycling of their aglycones and anthracyclineiron complexes (7). Other suggested contributing factors to DOX cardiotoxicity comprise platelet-activating factor, prostaglandins, histamine, calcium, and C-13 hydroxy anthracycline metabolites, etc. (8,9). DOX is metabolized to doxorubicinol, which is implicated for its cardiotoxicity, possibly by causing perturbation of the iron homeostasis (4).
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Lei Xi (2016) conducted an editorial in Doxorubicin cardiotoxicity. Visnagin was evaluated. Visnagin is highlighted as a potential protectant against doxorubicin-induced cardiotoxicity, which is primarily driven by oxidative stress and altered mitochondrial energetics.
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