Endometrial receptivity in polycystic ovary syndrome: altered biomarkers and underlying mechanisms

Polycystic ovary syndrome (PCOS) is a common endocrine disorder characterized by hyperandrogenism and ovulatory dysfunction. Women with PCOS are at an increased risk for adverse pregnancy outcomes, such as miscarriage and preterm birth. Endometrial receptivity plays a pivotal role in embryo implantation. However, there has been limited review or discussion regarding potential alterations in endometrial receptivity in PCOS patients, the nature of these changes, and their underlying mechanisms. In this review, we aim to summarize the alterations in endometrial receptivity associated with PCOS, highlight the impact of PCOS on endometrial receptivity, and explore the underlying mechanisms. Abnormal expression of key receptivity markers has been observed in both PCOS patients and animal models, which may contribute to reduced endometrial receptivity. The factors leading to impaired endometrial receptivity in PCOS are multifaceted, including hormonal imbalances, metabolic disturbances, chronic inflammation, and microbiota alterations. However, the intricate mechanisms behind PCOS-related endometrial dysfunction remain poorly understood. Further research is essential to unveil these complex mechanisms and improve fertility outcomes for women with PCOS.