Effects of Polyendocrine Metabolic Ovarian Syndrome (PMOS) on the Endometrium

Polyendocrine metabolic ovarian syndrome (PMOS), previously known as polycystic ovary syndrome (PCOS), is the most common reproductive, endocrine, and metabolic disorder affecting 11-13% of adolescent girls and women of reproductive age. Although anovulation has traditionally been considered the primary cause of PMOS-associated infertility, accumulating evidence demonstrates that impaired endometrial receptivity and decidualization also contribute substantially to embryo implantation failure, recurrent pregnancy loss, and other adverse pregnancy outcomes, including miscarriage, gestational diabetes, pregnancy-induced hypertension, preeclampsia, and preterm birth. In addition to reproductive disorders, women with PMOS also commonly present with obesity, insulin resistance, and other long-term health conditions. This review summarizes current knowledge of the cellular and molecular mechanisms by which PMOS disrupts endometrial function. We discuss how hyperandrogenism, insulin resistance, obesity, and chronic inflammation, both independently and collectively, impair endometrial receptivity by altering androgen receptor (AR) signaling, glucose metabolism, extracellular matrix (ECM) remodeling, immune homeostasis, cell-cell junctions, adhesion molecules, and key regulators of decidualization. We also highlight recent advances in transcriptomic and single-cell sequencing studies that have revealed cell type-specific alterations and molecular heterogeneity within the PMOS endometrium. Despite substantial progress, the mechanisms linking endocrine and metabolic abnormalities to impaired endometrial function remain incompletely understood. A better understanding of PMOS-associated endometrial dysfunction will facilitate the identification of novel therapeutic targets and improve embryo implantation success, pregnancy outcomes, and reproductive health in women with PMOS.