In recent decades, the Russian government has been committed to improving the country's demographic situation. Therefore, obstetricians and gynecologists pay special attention to women of reproductive age, whose reproductive system disorders can lead to infertility and the inability to conceive. Menstrual cycle disorders (MCDs) are a manifestation of various pathological conditions associated not only with disorders of the female reproductive system but also with general systemic and endocrine diseases. Since the 1980s, the incidence of MCDs has increased more than sevenfold. MCDs are characterized by changes in the cycle frequency, duration, and volume of menstrual blood loss. An obstetrician/gynecologist who initially consults a woman of reproductive age with MCDs should not only develop an examination plan for the patient, but most importantly, collect a detailed medical history, including a description of her physical condition, sports history, dietary habits, medication intake, including vitamins and dietary supplements, and analyze the relationship between MCDs and epigenetic factors in the woman's life. The incidence of NMC in the presence of an endocrine disease is up to 35% and requires referral of the patient to an endocrinologist to compensate for the endocrinopathy.

Age-related infertility has become the primary determinant of reproductive failure in modern societies due to a growing mismatch between biological and social fertility timelines. Accordingly, this review, adopting a uniquely holistic perspective, highlights the critical intersection between the demographic shift towards delayed parenthood and the physiological limitations of female reproductive aging, aiming to synthesize both established practices and the most promising regenerative frontiers. Reproductive aging involves a multifactorial decline across ovarian, uterine and tubal microenvironments, characterized by follicular depletion, oocyte aneuploidy, mitochondrial dysfunction, chronic inflammation, and structural macro- and microarchitectural modifications. While oocyte and ovarian tissue cryopreservation remain the most effective established clinical strategies, their success is strictly age-dependent and cannot reverse underlying cellular deterioration. The decline of the reproductive tract mirrors general organismal aging. Consequently, research is shifting towards new pharmacological interventions and regenerative approaches, such as coenzyme Q10, platelet-rich plasma, stem-cell-based therapies and artificial ovary development. These advancements suggest that future fertility preservation will adopt a holistic, anti-aging perspective, aimed at extending reproductive longevity as part of general organismal health. Additional research is needed to establish the long-term safety and clinical efficacy of these emerging experimental technologies before they can be integrated into routine practice.

Disorders of gonadotropin pulsatility contribute to reproductive dysfunction in humans and are often associated with metabolic dysfunction. Hypogonadotropic hypogonadism is characterized by chronically insufficient gonadotropin hormone production, leading to reproductive and metabolic impairments, such as infertility and obesity. Polycystic ovary syndrome (PCOS) is characterized by accelerated gonadotropin hormone production leading to reproductive and metabolic deficits, including oligomenorrhea, infertility, and an increased risk of type 2 diabetes mellitus. Hypothalamic kisspeptin is a key regulator of gonadotropin secretion, and disruptions in kisspeptin signaling result in abnormal gonadotropin pulsatility. Emerging evidence also implicates kisspeptin in energy metabolism. This study investigates the neuroendocrine mechanisms by which kisspeptin within KNDy neurons influences metabolic homeostasis. Using a Pdyn-Cre/Kiss1fl/fl knock-out (Kiss1Pdyn KO) mouse model, we combined diet-induced obesity, metabolic testing, and ovarian hormone depletion to assess the role of KNDy neuron kisspeptin in metabolic regulation and the interaction with sex steroids. Peripheral metabolism was more severely impacted in Kiss1Pdyn KO females than in KO males, with greater reproductive deficits observed in females. Abnormal glucose metabolism was partly attributable to the lack of ovarian steroids. Our findings indicate that loss of KNDy neuron kisspeptin in females promotes obesity through reduced energy expenditure without altering feeding behavior. Furthermore, this study identifies a female-biased role for KNDy kisspeptin as a central integrator of reproductive and metabolic signals.

RNA binding protein RBM46, as an integral component of MEIOC-YTHDC2 complex, governs the RNA binding specificity in posttranscriptional regulation of male meiotic initiation. RBM46 is also indispensable for embryonic oocyte development in mice. However, the precise phenotypic consequences and underlying regulatory mechanisms of RBM46 in female germ cells remain largely uncharacterized. Here, we demonstrate that RBM46 deficiency leads to derepression of CCNA2, meiotic arrest at leptotene stage and widespread germ cell apoptosis in embryonic ovaries. Transcriptomic profiling of RBM46-deficient ovaries at embryonic day 16.5 revealed significant upregulation of Stra8 and Lin28a, alongside downregulation of multiple meiotic genes. In HEK293T cells, ectopic co-expression of RBM46, MEIOC and YTHDC2 promoted degradation of reporter mRNAs bearing either Lin28a or Mga 3'UTR. Notably, Deletion of the RBM46-binding motif "AAUCAU" within Lin28a 3'UTR reduced this repressive effect. Collectively, these findings establish an essential role of RBM46 for meiotic initiation in female germ cells and identify Lin28a and Mga transcripts as direct targets subject to RBM46-mediated decay.