Endometriosis and endometrial cancer are distinct gynecological conditions that share overlapping biological mechanisms with implications for clinical management. Endometriosis is a chronic, benign disorder characterized by the ectopic implantation of functional tissue lining the uterus, primarily affecting women of reproductive age. It commonly causes chronic pelvic pain, dysmenorrhea, dyspareunia, and infertility. The disease is marked by persistent inflammation, hormonal dysregulation, and alterations in cellular signaling, which mirror some neoplastic processes despite lacking malignant potential. Endometrial cancer is a malignant tumor of the uterine lining, most frequently diagnosed in postmenopausal women. Its incidence is rising due to aging, obesity, and prolonged estrogen exposure. Epidemiological studies suggest a modest increase in endometrial cancer risk among women with endometriosis. However, detection bias and metabolic confounders may influence this association. Both conditions share estrogen dependence, chronic inflammatory microenvironments, and dysregulated pathways such as PI3K/AKT/mTOR. Somatic mutations in genes, including PTEN and ARID1A, further underline molecular intersections. Clinical management is tailored to disease type and severity. Endometriosis therapy emphasizes stepwise hormonal treatment, multidisciplinary pain management, and surgery when indicated. Endometrial cancer management relies on staging, with particular emphasis on molecular classification and histopathology to guide surgery, radiotherapy, chemotherapy, hormone therapy, and immunotherapy in advanced cases. Emerging noninvasive biomarkers and precision medicine strategies may enhance diagnosis, monitoring, and targeted treatment in both conditions. Understanding their shared and divergent mechanisms aids risk stratification, individualized therapy, and improved quality of life. Further prospective studies are needed to optimize patient-specific management and translate mechanistic insights into clinical practice.

Dysbiosis of the female genital tract microbiota represents a key pathological basis underlying clinical symptoms such as vaginal dryness and dyspareunia, which subsequently contribute to diminished sexual quality of life (QoL) in women. Although conventional antimicrobial therapies may provide short-term relief from infectious symptoms, they often fail to restore vaginal microbial homeostasis-thereby exhibiting inherent limitations, including high recurrence rates and increased risks of antimicrobial resistance. Vaginal microbiota transplantation (VMT), an emerging ecological restoration strategy, aims to reconstitute the recipient's vaginal microbiota by transferring a complete, functionally intact microbial community from a rigorously screened healthy donor. This review systematically delineates the multidimensional mechanistic links between genital tract dysbiosis and impaired female sexual quality of life; elucidates the core clinical value of VMT; comprehensively summarizes recent advances in both preclinical research and clinical trials; and critically examines major challenges currently facing the field-including the lack of standardized donor screening criteria, variability in procedural protocols, insufficient long-term safety data, and evolving ethical and regulatory considerations. Furthermore, we propose forward-looking perspectives on future directions, such as the development of individualized, precision-based VMT approaches; the establishment of standardized, evidence-based technical frameworks; and the acceleration of clinical translation and implementation. This review is intended to provide a robust theoretical foundation and practical guidance for the scientifically sound promotion, standardized application, and further investigation of VMT-ultimately advancing women's reproductive health and holistic sexual well-being.

Postmenopausal women often experience sexual dysfunction (e.g., vaginal dryness, dyspareunia) due to estrogen decline. While hormone replacement therapy (HRT) is effective, safety concerns have spurred interest in alternatives like soy isoflavones. This meta-analysis evaluated soy isoflavones' efficacy for sexual function and menopausal symptoms. We systematically searched PubMed, Cochrane, Scopus, and Web of Science through May 2025 per PRISMA guidelines, identifying 13 RCTs (n = 1325) comparing soy isoflavones (40-160 mg/day) with placebo/HRT. Outcomes included Menopause Rating Scale (MRS) scores. Risk of bias (Cochrane ROB-2) and heterogeneity (I[2]) were assessed. Soy isoflavones significantly improved vaginal dryness (SMD = - 1.88; 95% CI: -3.24 to -0.53; p = 0.006) and urogenital symptoms (SMD = - 0.33; 95% CI: -0.64 to -0.02; p = 0.04), with non-significant trends for vasomotor (p = 0.08) and psychological symptoms (p = 0.06). Effects were dose-dependent (optimal at 50-100 mg/day) and more pronounced in Asian populations. High heterogeneity (I[2] > 90%) reflected variability in study designs. Soy isoflavones appear safe and moderately effective for urogenital and sexual symptoms, though further standardized trials are needed to confirm long-term benefits.