Reproductive Sciences最新文献

In the intricate landscape of health disorders in women, polycystic ovary syndrome and endometriosis stand out. Despite their complete etiology being unknown, their impact on women's health and link to hereditary factors have given them the spotlight in the world of gynaecology and endocrinology. These two conditions although vastly different, share common symptoms, clinical manifestations, pathways and genetic and epigenetic factors and regulators [10, 39]. Decoding the link between the two conditions can lead to enormous breakthroughs in the diagnostic and therapeutic aspects of gynaecological disorders and possibly aid in the unravelling of unknown mechanisms associated with the pathophysiology of PCOS and endometriosis. MicroRNAs being small and potent regulators of gene expression, are infamous for their role in regulation of mRNA expression and aiding in post transcriptional modifications and their association with gynaecological disorders and impact on the endocrine system, typically the Hypothalamic-Pituitary-Ovarian axis has garnered an enormous amount of attention. MicroRNAs are known to affect pathways linked to inflammation, immunity, neuroendocrine stress response, fertility, metabolism, environmental response and are actively associated with the clinical manifestations of a plethora of diseases and disorders [37, 49-51]. This comprehensive review showcases the multifaceted roles of microRNAs involved in gynaecological disorders, specifically PCOS and endometriosis, offering avenues for microRNAs as possible therapeutic and diagnostic markers in gynaecological disorders, harnessing their applications to the maximum extent, possibly aiding in betterment of overall health in women.

Endometriosis (EMS) is a non-cancerous invasive condition where tissue resembling the lining of the uterus is found outside of the uterine cavity. Endometriotic lesions have been found in nearly every organ of the body. This review highlights examples of EMS exhibiting all eight established hallmarks of cancer: hyperproliferation (e.g. through estrogen signalling), evasion of growth suppression (e.g. through progesterone resistance), immunosurveillance evasion (e.g. through reduction of natural killer cell cytotoxicity), enabling replicative immortality (e.g. through increased telomere length), invasion (e.g. through epithelial-to-mesenchymal transition), induction of angiogenesis (e.g. through upregulation of hypoxia-inducible factors), resistance to apoptosis (e.g. through increased expression of survivin), and deregulation of cellular metabolism (e.g. through increased production of lactate). Therefore, despite being considered a non-cancerous, benign condition, EMS is highly cancer-like in its behaviours to promote invasion and ectopic survival. The presence of all hallmarks of cancer amongst endometriotic behaviours highlights that to expand understanding of endometriotic metastasis, as well as potential modes for management of EMS, it may be possible to leverage the larger knowledge base associated with cancer.

Our study aimed to investigate the association between chronic endometritis (CE) and thyroid peroxidase antibody (TPOAb) positivity, and to evaluate the effect of antibiotic therapy on assisted reproductive technology (ART) outcomes in patients with TPOAb-positive CE. A total of 1,385 women undergoing ART were enrolled and categorized into TPOAb-negative (n = 1,240) and TPOAb-positive (n = 145) groups. The prevalence of CE was significantly higher in the TPOAb-positive group compared with the TPOAb-negative group (62.76% vs. 43.47%, p < 0.001). At our center, patients diagnosed with CE routinely received antibiotic therapy prior to ART. In subgroup analyses restricted to CE patients, with clinical pregnancy rate (CPR) and live birth rate (LBR) as the primary outcomes, TPOAb-positive patients with CE who received antibiotics showed significantly higher CPR (52.75% vs. 41.37%, p = 0.0426) and LBR (48.35% vs. 35.44%, p = 0.0184). These associations remained robust after adjustment for potential confounders. In conclusion, TPOAb positivity is linked to a higher prevalence of CE, and antibiotic therapy prior to ART improves reproductive outcomes in TPOAb-positive patients with CE.

Nesfatin-1 is a peptide hormone that is commonly associated with appetite regulation and is primarily expressed in the brain. However, it has recently been identified in various peripheral organs, including the ovaries and uterus. This study aimed to investigate the expression and functional role of nesfatin-1 in the mouse endometrium. Due to the lack of established mouse endometrial cell lines, a primary culture system was developed by isolating endometrial cells through enzymatic digestion, enabling in vitro analyses. We examined the presence and regulatory potential of nesfatin-1 in these cells, focusing particularly on endometrial decidualization, a critical process for implantation and pregnancy maintenance. Our results revealed that nesfatin-1 and its binding sites are expressed in mouse endometrial cells. Furthermore, Nucb2 mRNA expression was significantly increased following estradiol treatment but not progesterone treatment, suggesting hormone-specific regulation of nesfatin-1 expression. Notably, nesfatin-1 treatment to mouse endometrial cells resulted in a significant upregulation of decidualization-associated genes, including prolactin family 8, subfamily a, member 2 (Prl8a2), alkaline phosphatase (Alpl), and bone morphogenetic protein 2 (Bmp2). Furthermore, in a delayed implantation mice model, there was a significant decrease in Nucb2/nesfatin-1 expression and decidualization-associated genes. Importantly, nesfatin-1 administration restored the expression of these genes in the delayed implantation conditions. Taken together, these findings demonstrate that nesfatin-1 plays a pivotal role in promoting endometrial decidualization and successful implantation, suggesting its potential as a therapeutic target for enhancing fertility and improving pregnancy outcomes.

This study explores the molecular mechanisms driving recurrent spontaneous abortion, a condition affecting 1-5% of women of reproductive age, with 40-50% of cases unexplained. Focusing on endometrial cell senescence, a process linked to irreversible cell cycle arrest, the research identifies uncoupling protein 2 (UCP2) and glutathione reductase (GSR) as key contributors to this pathology. By analyzing transcriptome data from the Gene Expression Omnibus database, 21 genes associated with cellular senescence were found to be differentially expressed, with UCP2 and GSR significantly upregulated. These findings were validated using a hydrogen peroxide-induced senescence model in human endometrial stromal cells. Diagnostic potential was confirmed through receiver operating characteristic curve analysis, showing promising results for both UCP2 and GSR. The study also observed increased activity of natural killer and T cells in affected tissues, pointing to an immune component in recurrent spontaneous abortion. Drug prediction analysis highlighted dexamethasone and menadione as potential treatments. These insights suggest that oxidative stress-induced senescence plays a critical role in recurrent spontaneous abortion, with UCP2 and GSR as promising biomarkers and therapeutic targets to improve endometrial health and reduce miscarriage risk. Further clinical studies are needed to validate these findings and explore their therapeutic applications.