Key result
Doxorubicin treatment in mice induced significant reactive oxygen species production in the left heart but not the right, with transcriptional changes correlating with myocardial dysfunction.
Why the study?
Heart failure limits doxorubicin use in cancer therapy, prompting investigation into differential left and right ventricular gene expression profiles in mice with preserved versus impaired myocardial function.
Does doxorubicin induce differential transcriptional changes and ROS production in the left and right ventricles of mice with preserved vs impaired cardiac function?
Population
48 male mice
Comparison
Doxorubicin responding vs non-responding animals
Design
Preclinical animal study
Follow-up
One week after the final dose
Authors
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May identify targets against doxorubicin cardiotoxicity; leaves open clinical translation pending prospective validation.
Does doxorubicin induce differential transcriptional changes and ROS production in the left and right ventricles of mice with preserved vs impaired cardiac function?
Doxorubicin induces differential gene expression and ROS production in the left versus right heart, correlating with the occurrence of myocardial dysfunction in a mouse model.
Stamm et al. (2021) studied Doxorubicin-induced heart failure (n=48). Doxorubicin was evaluated on Reactive oxygen species (ROS) production and gene expression profiling. Doxorubicin treatment in mice induced significant reactive oxygen species production in the left heart but not the right, with transcriptional changes correlating with myocardial dysfunction.
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