Key result
Dexrazoxane pre-treatment prevents daunorubicin-induced histopathologic lesions and RyR2 mRNA decreases in rats.
Why the study?
Anthracycline cardiotoxicity involves decreased expression of Ca(2+)-handling proteins such as the ryanodine receptor, and the effect of dexrazoxane on this gene expression was unknown.
Does dexrazoxane prevent the down-regulation of ryanodine receptor gene expression in anthracycline-induced cardiomyopathy in rats?
Population
Rats treated chronically with daunorubicin
Comparison
Dexrazoxane pre-treatment vs daunorubicin alone and control rats
Design
Preclinical experimental study
Follow-up
6 weeks
Authors
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Supports RyR2 preservation as a cardioprotective mechanism; leaves open translation to human anthracycline cardiomyopathy.
Does dexrazoxane prevent the down-regulation of ryanodine receptor gene expression in anthracycline-induced cardiomyopathy in rats?
Dexrazoxane prevents the down-regulation of ryanodine receptor gene expression and histopathologic lesions in a rat model of anthracycline-induced cardiomyopathy.
Burke et al. (2000) studied Anthracycline cardiomyopathy. Dexrazoxane vs. Daunorubicin alone was evaluated on RyR2/GAPDH mRNA ratio and histopathologic lesions. Dexrazoxane pre-treatment prevented the daunorubicin-induced decrease in RyR2/GAPDH mRNA ratio and histopathologic lesions in rats.
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