Reproductive Sciences最新文献

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.

Oligoasthenozoospermia (OAT) is a major cause of declining male fertility worldwide, characterized by reduced sperm count and motility. Its pathogenesis involves multiple factors including genetics, hormones, environment, and lifestyle. Due to ethical and practical limitations in human studies, animal models have become essential tools for elucidating OAT mechanisms and evaluating therapeutic strategies. This review aims to systematically organize and evaluate existing OAT animal models, including those established through chemical agents, heavy metals, endocrine disruptors, physical stress, genetic modification, and nutritional imbalance. It summarizes these models based on their mechanistic foundations, phenotypic characteristics, advantages, and limitations. Results indicate that despite significant research advances, existing models remain limited in standardization, depth of mechanism elucidation, and clinical translational value. Therefore, future efforts should focus on developing more comprehensive and clinically relevant animal models to deepen understanding of OAT pathophysiology and advance the development of effective and personalized therapeutic strategies.