Key result
Juvenile exposure to doxorubicin in mice impaired vascular development and progenitor cell function, resulting in greater susceptibility to stress-induced myocardial injury and rapid heart failure.
Why the study?
Does juvenile exposure to doxorubicin impair cardiac progenitor cell function and vascularization, increasing susceptibility to stress-induced myocardial injury in adult mice?
Population
Juvenile mice
Design
Preclinical
Follow-up
Until adulthood
Authors
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Hypothesis-generating for vascular mechanisms of late cardiotoxicity; leaves open translation to pediatric survivors.
Does juvenile exposure to doxorubicin impair cardiac progenitor cell function and vascularization, increasing susceptibility to stress-induced myocardial injury in adult mice?
Juvenile exposure to doxorubicin impairs cardiac vascular development and progenitor cell function, providing a mechanism for the increased susceptibility of the adult heart to stress-induced injury and late-onset cardiotoxicity.
Huang et al. (2010) studied Late-onset doxorubicin-induced cardiotoxicity. Doxorubicin was evaluated on Vascular development, progenitor cell function, and susceptibility to stress-induced myocardial injury. Juvenile exposure to doxorubicin in mice impaired vascular development and progenitor cell function, resulting in greater susceptibility to stress-induced myocardial injury and rapid heart failure.
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