From Nutrient to Signaling Molecule: Uridine Ushers in a New Era of Reproductive Anti-Aging

In the field of reproductive medicine in 2026, research on female fertility preservation has achieved a landmark breakthrough. Recently, a landmark study published in Nature Communications revealed that uridine can markedly restore the quality of aged oocytes and delay reproductive aging. Conducted collaboratively by teams from Peking University Third Hospital, Zhejiang University and other institutions, this study provides novel theoretical support for addressing fertility challenges in advanced-age women.

Metabolomic analysis by the research team found that uridine levels are significantly diminished in aged mice. Experimental data show that uridine supplementation not only substantially improves meiotic maturation, fertilization capacity and early embryonic development of oocytes, but also raises the average litter size of aged mice by approximately 74%. The underlying molecular mechanism is particularly critical: as a ligand, uridine directly binds to the PCBP1 protein and inhibits the ferroptosis pathway, thereby effectively alleviating mitochondrial dysfunction and oxidative damage.

This finding overturns conventional understanding and confirms that uridine is not merely a nutrient, but also a key signaling molecule regulating reproductive aging. For the biomedical industry, this indicates that targeting PCBP1 or supplementing uridine metabolic precursors enables the development of a new generation of assisted reproductive interventions, boasting outstanding clinical translational value.

FOR DETAIL：https://www.nature.com/articles/s41467-026-72406-8

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