Reproductive Sciences最新文献

The uterine cavity was formerly considered sterile; however, over recent years, researchers have identified the presence of endometrial microbiota. An imbalance in the endometrial microbiota, or dysbiosis, has been shown to be associated with a variety of gynecological diseases. Endometriosis (EM) is a chronic and inflammatory gynecological disease that affects 6-10% of all women of reproductive-age. Previous studies suggested that endometrial dysbiosis can participate in the development of EM by generating an inflammatory state, leading to disorders of immune homeostasis and thus creating an intrauterine environment conducive to endometrial stromal cell migration and adhesion. In this review, we investigate differences in the endometrial microbiota of patients with EM compared with that of healthy women and discuss the possible pathogenic mechanisms responsible for endometrial dysbiosis. Critically, we identified that an increase of lipopolysaccharides resulting from microbiological disorders may generate chronic inflammation, leading to increased adhesion and angiogenesis, and the development of EM. The findings of our review may identify new therapeutic strategies and potential therapeutic targets for EM.

Primary ovarian insufficiency (POI) is a multifactorial disorder marked by ovarian function cessation before age 40, leading to infertility and systemic complications, including osteoporosis, cardiovascular disease, and neurocognitive impairment. It results from accelerated ovarian reserve depletion, impaired folliculogenesis, and hormonal dysregulation. The majority of cases are idiopathic, with known causes including genetic mutations, autoimmune disorders, infections, and iatrogenic factors. Recent RNA sequencing advances highlight microRNAs (miRNAs) as critical regulators of ovarian processes. Dysregulated miRNAs drive granulosa cell apoptosis, oxidative stress, and follicular atresia, with distinct profiles offering potential as biomarkers for early diagnosis and therapeutic targets. This review synthesizes miRNA-mediated mechanisms in POI, integrating their roles in apoptosis, DNA repair, and folliculogenesis, and evaluates miRNA-based diagnostics and therapies, including exosome-mediated delivery, to improve reproductive and clinical outcomes.

Human papillomavirus (HPV) and Chlamydia trachomatis (CT) co-infection is increasingly recognized not as a mere coincidence, but as a synergistic partnership that accelerates oncogenic progression across multiple tissues. This review synthesizes existing evidence into a "central-peripheral" framework, positioning cervical cancer as the central, mechanistically well-established model of cooperation, while malignancies such as head and neck, ovarian, and breast cancers represent the emerging, though less substantiated, peripheral extensions. This synthesis delineates an emerging paradigm of bidirectional interplay: CT fosters a permissive microenvironment for HPV persistence by impairing host immunity and inducing chronic inflammation, while HPV oncoproteins promote tumorigenesis by disrupting tumor suppressor functions and reprogramming cellular metabolism. These resulting metabolic alterations in the host cell form the basis for the hypothesis of a metabolic co-dependency that may further reinforce CT persistence. The convergence of these pathogens on shared pathways, specifically immune evasion, genomic instability, and metabolic reprogramming, outlines a synergistic network. However, definitive proof of causality, particularly for the bidirectional effects in non-cervical cancers, remains constrained by methodological heterogeneity. Bridging these gaps requires future research to leverage immunocompetent co-infection models and multi-omics approaches. Elucidating the HPV-CT interactome supports a conceptual shift from a single-pathogen to a multi-pathogen oncogenesis model, which is pivotal for developing the next generation of precision prevention and therapy.