Polycystic ovary syndrome (PCOS) is a common endocrine disorder in women of reproductive age and is characterized by excessive androgen levels and ovulatory dysfunction. PCOS with a wide range of heterogeneous syndromes affects the health of a large part of the female population of the world.PCOS is a complex endocrinopathy that includes a variety of symptoms, such as menstrual disorders, infertility, acne, hirsutism, and several metabolic disorders. Given the different clinical manifestations, unknown etiology, and complex pathophysiology, the diagnosis of PCOS is still controversial.The prevalence of PCOS is often estimated between 2% and 26%. This significant difference in prevalence may be due to differences in diagnostic criteria, sample heterogeneity, socioeconomic status, access to health care, and general health awareness. Furthermore, given the multiple phenotypes of PCOS and the fact that it is predominantly diagnosed by gynecologists and endocrinologists, while it is poorly studied in other specialties and primary care physicians, these estimates may sometimes be lower.The article is a review of the scientific literature on various pathogenetic aspects of the development of PCOS, which arises as a result of polygenic susceptibility in combination with environmental influences, which may include epigenetic changes and intrauterine programming. Racial and ethnic differences may influence clinical manifestations through the genetic and environmental predisposition to endocrinopathies and metabolic diseases. In addition to the well-known clinical manifestations of hyperandrogenism and ovulatory dysfunction, women with PCOS are at increased risk for adverse mental health outcomes, pregnancy complications, and cardiometabolic disease.Treatment methods have limited effectiveness, mostly due to the fact that the development of drugs is difficult by an incomplete definition of the main pathophysiological processes. Advances in adipocyte genetics, metabolomics, and structure have improved understanding of key changes in neuroendocrine, enteroendocrine, and steroidogenic pathways, including increased gonadotropin-releasing hormone pulsatility, androgen excess, insulin resistance, and changes in the gut microbiome.Many patients have high levels of 11-oxygenated androgens with high androgenic activity, which may pose a metabolic risk. These advances have prompted the development of new therapies, including those targeting the neurokinin–kispeptin axis upstream of gonadotropin-releasing hormone, with the potential to reduce adverse clinical outcomes and improve patient outcomes.