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- W2069173844 abstract "This editorial refers to ‘Adiponectin protects against doxorubicin-induced cardiomyopathy by anti-apoptotic effects through AMPK up-regulation’ by M. Konishi et al. , pp. 309–319, this issue.Doxorubicin, an anthracycline drug widely used for the treatment of various solid-organ tumours and haematological malignancies, has significant cardiac toxicity that limits its utilization. Doxorubicin can cause both an acute and a chronic form of cardiotoxicity and heart failure. Chronic cardiotoxicity, which ranges from an incidence of ∼1% at a cumulative dose of 550 mg/m2 to >30% at cumulative doses above 560–1160 mg/m2, can occur at any time after initiation of treatment and even years after cessation of therapy.1 The clinical presentation is that of classic progressive idiopathic heart failure, with histological evidence of cardiac damage defined by swelling of the sarcoplasmic reticulum and myofibrillar loss. However, the occurrence of doxorubicin-induced cardiotoxicity can vary widely regardless of cumulative drug dosage, and the assessment of parameters that modify risk is of great interest. Doxorubicin-induced cardiotoxicity and heart failure can also be induced in mice, presenting a model system to identify the mechanisms by which doxorubicin-induced heart failure occurs and to test therapeutic approaches by which this toxicity may be prevented.Despite the availability of model systems, the anti-neoplastic and cardiotoxic mechanisms of doxorubicin are not entirely clear. Doxorubicin is reduced by NADPH oxidase2 to a semi-quinone free radical that can, in the presence of iron, interact with oxygen to …" @default.
- W2069173844 created "2016-06-24" @default.
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- W2069173844 date "2010-12-14" @default.
- W2069173844 modified "2023-09-24" @default.
- W2069173844 title "Fighting doxorubicin-induced cardiotoxicity with adiponectin" @default.
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- W2069173844 doi "https://doi.org/10.1093/cvr/cvq393" @default.
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