We used to think post-menopausal ovaries just sat there quietly after their reproductive job was done. New research in mice suggests they may instead undergo an identity shift from reproduction to inflammation. A team led by Francesca Duncan at Northwestern University found that ovaries in aged mice lose their egg-producing follicles and dial down genes linked to: At the same time, genes tied to inflammation and immune activity ramp up. The ovaries also become infiltrated with more immune cells such as: In a related (not-yet-peer-reviewed) study of post-menopausal women aged 50–75, the researchers saw the ovaries’ molecular signatures continue changing dramatically over the decades. The organ is not stagnant. Read more Duncan suspects the post-reproductive ovary may contribute to “inflammaging”, the chronic, low-grade inflammation that accompanies aging. “It’s losing the reproductive signature and taking on an immune signature, but I don’t think that’s necessarily a good thing,” Duncan says. Mice don’t experience menopause exactly like humans, but they do undergo age-related fertility decline and hormonal changes. Experts note key similarities (follicle depletion, fibrosis, etc.) that make the findings relevant. If the same shift occurs in people, it could help explain why inflammation-related conditions (like rheumatoid arthritis) often increase after menopause. Bottom line: the post-menopausal ovary may be more active than we thought. Read more
- reproduction
- estrogen production
- T cells
- Macrophages
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