Fisetin reduced old mouse plasma’s harmful effects on arteries
Peak dilation of isolated mouse arteries was 14% higher with plasma from fisetin-treated old mice than with plasma from old mice given a control solution.
Randomized, dose-response
Limit: Only 2–3 mice per sex and treatment group in the gene-activity analysis
Edited by Boris Djordjevic · AgingResearch.News
Male and female C57BL/6N mice aged 6 or 27 months were randomly assigned to fisetin or a control solution in an animal experiment. Researchers gave fisetin orally at 100 milligrams per kilogram daily for one week, followed by two weeks off and another week on.
In old mice, fisetin reduced activity of the gene for CXCL12, a signaling protein, in senescent vessel-lining cells. Senescence is a state in which cells stop dividing. Fisetin also reduced age-related elevations in circulating CXCL12. Isolated arteries from young mice widened less after 24 hours of exposure to plasma, the liquid part of blood, from old control mice. Plasma from fisetin-treated old mice caused less impairment. Adding CXCL12 back to this plasma reduced artery widening. The authors concluded that CXCL12 partly mediated the plasma’s harmful effects.
Why it matters
Understanding how secretions from senescent cells affect blood vessels may help identify targets for research on age-related cardiovascular disease.
Caveats
The functional experiments used isolated mouse arteries and human aortic lining cells grown in the lab, not cardiovascular outcomes in people. The gene-activity analysis used aortas from 2–3 mice per sex and treatment group.
The paper
University of Colorado Boulder
Aging Cell, Apr 23, 2026, Open access
