Fisetin compound restores immune cell function and physical performance in aging, study finds
Researchers found that fisetin, a plant-derived compound, restores MYC protein expression in macrophages and improves immune function and physical performance in aging organisms. The study demonstrates that reduced MYC levels drive age-related decline in macrophage function, a key component of innate immunity. The findings suggest a potential therapeutic target for reversing immune aging and age-related frailty.
A bioRxiv preprint reports that fisetin treatment restores MYC transcription factor expression in macrophages from older individuals, reversing age-related declines in pathogen phagocytosis and cell migration. The researchers used multiple model systems—Drosophila, human primary macrophages, and mice—to demonstrate that macrophage-specific MYC overexpression improves physical performance in aging flies and that fisetin feeding in older mice enhances motor activity and reduces frailty. Mechanistically, fisetin acts by restoring expression of MYC target genes that become dysregulated with age. While lifespan was not affected in the Drosophila model, the improvements in immune function and physical performance suggest potential clinical applications for age-related immune decline and frailty.
What's missing
The study's limitations include: results are from preclinical models and have not yet been tested in human clinical trials; the mechanism by which fisetin specifically activates MYC in macrophages requires further investigation; long-term safety and efficacy of fisetin supplementation in humans remain unknown; and whether improvements in macrophage function translate to clinically meaningful outcomes in aging populations has not been established.
What different sources said
- bioRxivCenter
Fisetin-mediated MYC restoration improves age-associated decline in macrophage function
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