Current trends in the research of the etiopathogenesis and treatment of endometriosis

Relevance. Endometriosis is a chronic disease characterized by the ectopic localization of endometrial tissue and is widely prevalent among women of reproductive age (up to 9%). The condition is associated with chronic pelvic pain, dysmenorrhea, dyspareunia, and infertility, leading to a significant reduction in quality of life and reproductive potential. Despite decades of research, the etiology and pathogenesis of endometriosis remain insufficiently understood, while existing treatment methods, including hormonal therapy and surgical intervention, often provide only temporary relief and are associated with adverse effects. Therefore, an in-depth investigation of the molecular mechanisms underlying endometriosis and the development of novel therapeutic approaches remains highly relevant. Aim. To summarize current data on the etiopathogenesis of endometriosis and to analyze promising directions for its treatment. Materials and methods. A review of Russian and international publications from the past five years was conducted using the elibrary and PubMed databases, as well as the clinical guidelines “Endometriosis” developed by the Russian Society of Obstetricians and Gynecologists. Results. The analysis revealed increased expression of estrogen receptor alpha (ERα) and decreased activity of estrogen receptor beta (ERβ) in endometriotic lesions, which contributes to enhanced tissue proliferation, inflammatory processes, and impaired immune response. Conclusion. The obtained data confirm the key role of hormonal imbalance, particularly alterations in the ERα/ERβ ratio, in the pathogenesis of endometriosis and highlight the potential of molecular targeted therapy. Further investigation of pathogenetic mechanisms may contribute to the development of effective treatment strategies and prevention of complications, including oncological transformation. Keywords: endometriosis, pathogenesis, conservative treatment, laparoscopy, progestins.