Douglas R. Seals

Senolytic treatment with fisetin reverses age-related endothelial dysfunction partially mediated by SASP factor CXCL12

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.

Integrated Multiomics Links Metabolic and Inflammatory Remodeling to Arterial Stiffness After the 4,486-km Trans Europe Footrace

This study links metabolic and inflammatory changes to arterial stiffness in ultra-endurance runners using multi-omics analysis of plasma samples.

Methylglyoxal-induced glycation stress promotes aortic stiffening: Putative mechanistic roles of oxidative stress and cellular senescence

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.

Cellular Senescence Mediates Doxorubicin Chemotherapy-Induced Vascular Endothelial Dysfunction: Translational Evidence of Prevention with Senolytic Treatment

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

Cellular Senescence Mediates Doxorubicin Chemotherapy-Induced Aortic Stiffening: Role of Glycation Stress

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.

Healthy aging interventions reduce non-coding repetitive element transcripts

The paper investigates how healthy aging interventions affect non-coding repetitive element transcripts in mice and humans, finding they are globally reduced by interventions and increased by aging.