The role of DNA methylation, histone modifications, and non-coding RNA expression in the pathogenesis of premature ovarian insufficiency and innovative ways to overcome infertility from the point of epigenetic disturbances

Premature ovarian insufficiency (POI) is a multifactorial and heterogeneous condition characterized by secondary amenorrhea, elevated levels of follicle-stimulating hormone (FSH), and decreased levels of estradiol and anti-Müllerian hormone (AMH). The etiology of POI is influenced by genetic, epigenetic, autoimmune, environmental, and other factors. Epigenetic mechanisms, such as DNA methylation, histone modifications, and regulation by non-coding RNAs, play a significant role in the pathogenesis of POI. Hypermethylation of gene promoters (e.g., FOXO3, BMP15, GDF9) and alterations in histone modifications (e.g., H3K9ac, H3K27me3) lead to the suppression of genes involved in oogenesis and folliculogenesis. Non-coding RNAs, including microRNAs (e.g., miR-23a, miR-21) and long non-coding RNAs (e.g., HOTAIR), regulate processes such as apoptosis and oxidative stress in ovarian cells. The study of epigenetic mechanisms opens up new perspectives for the development of personalized approaches to the early diagnosis and treatment of IDD, which is especially important for women with infertility.