An Update on the Progress of Endometrial Receptivity in Women with Polycystic Ovary Syndrome

Polycystic ovary syndrome (PCOS) is a significant public health issue with diverse presentations, including reproductive, metabolic, and psychological disorders. Although problems with ovulation, metabolism, and hormonal imbalance can be pharmacologically improved, even the excellent quality of transferred embryos does not necessarily increase the pregnancy rate. Poor endometrial receptivity in women with PCOS perturbs endometrial decidualization and blastocyst implantation, increasing adverse pregnancy outcomes, such as miscarriage and poor embryonic development. The etiological and pathophysiological mechanisms involved in defective endometrial receptivity in women with PCOS have not been fully elucidated to date. Various contributing factors have been reported as primary causes of defective endometrial receptivity in women with PCOS, including metabolic alterations, inflammatory events, and some abnormally expressed endometrial molecular markers. However, few studies to date have investigated in depth the complex mechanisms underlying the compromised endometrial receptivity in women with PCOS. This article reviews recent reports mainly on metabolic alterations and some new endometrial molecular markers in order to collate the existing data and improve our understanding in this field. The aim was to discuss current novel insights on defective endometrial receptivity in women with PCOS in order to provide a theoretical basis for reducing adverse pregnancy outcomes and improving the live birth rate in PCOS.