Polycystic Ovary Syndrome (PCOS) is a common endocrine disorder affecting 5–15% of women of reproductive age, with many cases undiagnosed. It is characterized by hormonal imbalances, insulin resistance, and ovarian dysfunction, leading to irregular ovulation and fertility challenges. Despite restoring ovulation through medication, women with PCOS face lower pregnancy rates and higher risks of implantation failure and miscarriage. This review explores the complexities of PCOS in pregnancy, focusing on hormonal and metabolic imbalances that impair endometrial receptivity and decidualization. Disrupted estrogen signaling, reduced tight junction integrity, and progesterone resistance contribute to these issues. Immune cell dysregulation and inflammatory processes further complicate reproductive outcomes. The review also discusses rodent models induced by hormonal interventions, such as DHEA, DHT, and TP, which help elucidate PCOS mechanisms and potential treatments. These models reveal ovarian dysfunction, impaired endometrial receptivity, and decidualization defects. The interplay of hormonal, metabolic, and immune factors in PCOS significantly impacts pregnancy, highlighting the need for advanced understanding and targeted therapies to improve reproductive outcomes.Polycystic Ovary Syndrome (PCOS) is a common endocrine disorder affecting 5–15% of women of reproductive age, with many cases undiagnosed. It is characterized by hormonal imbalances, insulin resistance, and ovarian dysfunction, leading to irregular ovulation and fertility challenges. Despite restoring ovulation through medication, women with PCOS face lower pregnancy rates and higher risks of implantation failure and miscarriage. This review explores the complexities of PCOS in pregnancy, focusing on hormonal and metabolic imbalances that impair endometrial receptivity and decidualization. Disrupted estrogen signaling, reduced tight junction integrity, and progesterone resistance contribute to these issues. Immune cell dysregulation and inflammatory processes further complicate reproductive outcomes. The review also discusses rodent models induced by hormonal interventions, such as DHEA, DHT, and TP, which help elucidate PCOS mechanisms and potential treatments. These models reveal ovarian dysfunction, impaired endometrial receptivity, and decidualization defects. The interplay of hormonal, metabolic, and immune factors in PCOS significantly impacts pregnancy, highlighting the need for advanced understanding and targeted therapies to improve reproductive outcomes.