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Emerging evidence suggests that intrinsic endometrial defects play a critical role in PCOS\u2010associated infertility; however, the underlying molecular mechanisms remain poorly understood. In this study, we demonstrated that interleukin 22 (IL\u201022) signaling directly modulated endometrial function and that downregulation of the IL\u201022\u2010STAT3 pathway contributed to impaired endometrial receptivity in PCOS. Consistently, exogenous IL\u201022 administration in a PCOS\u2010like mouse model restored STAT3 phosphorylation and effectively alleviated implantation failure by enhancing endometrial receptivity. Mechanistically, we identified insulin\u2010like growth factor\u2010binding protein 5 (IGFBP5) as a direct downstream target of STAT3 in endometrial organoids derived from patients with PCOS. 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