Key result
Fenofibrate attenuated doxorubicin-induced cardiac dysfunction and significantly increased circulating endothelial progenitor cells (2% vs 0.5% of total events) in mice.
Why the study?
EPCs restore endothelial function in heart failure, prompting investigation into whether fenofibrate improves myocardial function via eNOS-mediated EPC activation in doxorubicin-induced cardiomyopathy.
Does fenofibrate improve myocardial function in a doxorubicin-induced cardiomyopathy mouse model?
Population
Wild-type mice with doxorubicin-induced cardiomyopathy
Comparison
Vehicle vs DOX + saline vs DOX + fenofibrate vs DOX + fenofibrate + L-NAME
Design
Animal experimental study
Follow-up
4 weeks
Authors
Loading...
Fenofibrate increases EPCs in DOX cardiomyopathy mice; leaves open clinical translation to human HF endothelial repair.
Does fenofibrate improve myocardial function in a doxorubicin-induced cardiomyopathy mouse model?
Absolute Event Rate: 2% vs 0.5%
p-value: p=<0.05
Fenofibrate ameliorates doxorubicin-induced cardiac toxicity in mice by promoting Akt/eNOS and VEGF to activate EPC pathways.
Huang et al. (2021) studied Doxorubicin-induced cardiomyopathy (n=53). Fenofibrate vs. Saline was evaluated on Circulating endothelial progenitor cells (EPCs) as a percentage of total events (p=<0.05). Fenofibrate attenuated doxorubicin-induced cardiac dysfunction and significantly increased circulating endothelial progenitor cells (2% vs 0.5% of total events) in mice.
Synapse has enriched 5 closely related papers on similar clinical questions. Consider them for comparative context: