Regular ArticleSarcoplasmic Reticulum Calcium Release Is Stimulated and Inhibited by Daunorubicin and Daunorubicinol
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2019, Journal of Biological ChemistryCitation Excerpt :Doxorubicin is member of the anthracycline drug class commonly used to treat a range of cancers and has attracted considerable attention because of its cardiotoxic side effects. Doxorubicin and its metabolite, doxorubicinol, also accumulate in skeletal muscle (1, 2), resulting in a myotoxicity, which can persist long beyond the cessation of treatment (3). Patients treated with doxorubicin frequently experience muscle atrophy (4, 5), as well as symptoms of muscle weakness and fatigue (6, 7).
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2018, Journal of Molecular and Cellular CardiologyCitation Excerpt :The increased production of ROS, in turn, induces lipid peroxidation leading to cardiomyocyte membrane damage. In addition, DOXO can enter the mitochondria causing increased Ca2+ current along with inhibition of sarcoplasmic reticulum function; decreased activity of Na+, K+-ATPase [5] release of cytochrome C and, finally, cardiomyocyte death generally by apoptosis [6]. Myofibrillar loss and cytoplasmic vacuolization, caused by dilation of the sarcoplasmic reticulum in myocardial cells, are the most common histological features found in anthracycline-induced cardiomyopathy.
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