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• W2327904433 abstract "Caveolin-1-deficient (cav1−/−) mice display a severely diseased cardiac phenotype with systolic and diastolic heart failure. Accumulating evidence supports a causative role of uncoupled endothelial nitric oxide synthase in the development of these abnormalities. Interestingly, a similar molecular mechanism was proposed for anthracycline-induced cardiomyopathy. Currently, dexrazoxane is approved for the prevention of anthracycline-induced cardiomyopathy. Given the molecular similarities between the anthracycline-induced cardiomyopathy and the cardiomyopathy in cav1−/− mice, we questioned whether dexrazoxane may also prevent the evolution of the cardiac pathologies in cav1−/− mice. We evaluated dexrazoxane treatment for 6 weeks in cav1−/− mice and wild-type controls. This study provides the first evidence for a reduced reactive oxygen species formation in the vessels of dexrazoxane-treated cav1−/− mice. This reduced oxidative stress resulted in a markedly reduced rate of apoptosis, which finally was translated into a significantly improved heart function in dexrazoxane-treated cav1−/− mice. These hemodynamic improvements were accompanied by significantly lowered proatrial natriuretic peptide levels. Notably, these protective properties of dexrazoxane were not evident in wild-type animals. Taken together, these novel findings indicate that dexrazoxane significantly reduces vascular reactive oxygen species formation cav1−/−. Because this is paralleled by an improved cardiac performance in cav1−/− mice, our data suggest dexrazoxane as a novel therapeutic strategy in this specific cardiomyopathy." @default.
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• W2327904433 date "2013-06-01" @default.
• W2327904433 modified "2023-09-25" @default.
• W2327904433 title "Dexrazoxane Prevents the Development of the Impaired Cardiac Phenotype in Caveolin-1-disrupted Mice" @default.
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• W2327904433 doi "https://doi.org/10.1097/fjc.0b013e31828de47c" @default.
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