Uterine factors in premature ovarian insufficiency
A critical knowledge gap in premature ovarian insufficiency (POI) can be filled by shifting the focus beyond ovarian dysfunction to systematically elucidate concomitant and intrinsic endometrial alterations.
POI induces profound, intrinsic pathological changes in the endometrium across histological, molecular, and functional levels, which may persist independently and are not solely attributable to low estrogen states.
Key endometrial molecular alterations include decreased expression of ERα, HOXA10, and FSHR, alongside a proinflammatory cytokine profile (elevated IFN-γ, IL2, and TNF-α, and reduced IL4) and increased uterine natural killer cell infiltration, providing a mechanism for compromised embryo implantation.
Emerging therapeutic strategies target specific endometrial abnormalities in POI to restore receptivity and improve fertility outcomes.
https://www.cell.com/trends/molecular-medicine/fulltext/S1471-4914(25)00280-1
