Sophia A. Mahoney

Single-cell aortic transcriptomics and plasma bioassays in aged mice show that intermittent fisetin treatment clears senescent endothelial cells and reverses endothelial dysfunction partially driven by circulating CXCL12.

This study shows that methylglyoxal-induced glycation stress causes aortic stiffening through oxidative stress and cellular senescence, and a glycation-lowering compound mitigates these effects.

This study shows that cellular senescence contributes to Doxorubicin-induced vascular endothelial dysfunction and that senolytic treatment can prevent this dysfunction.

This study shows that doxorubicin chemotherapy induces aortic stiffening via cellular senescence and the senescence-associated secretory phenotype, which can be mitigated by senolytic therapy.