Reproductive Sciences最新文献

{"title":"The KAT5-TSP-1 Axis Maintains Ovarian Redox Homeostasis and Is Impaired in Polycystic Ovary Syndrome.","authors":"Qiu Jin, Wei Yang, Chao Wang, Yu Liu, Ruijing Wang, Li Liu, Xianghan Zhang, Jin Yan, Meimei Liu","doi":"10.1007/s43032-026-02154-z","DOIUrl":"10.1007/s43032-026-02154-z","url":null,"abstract":"<p><p>Polycystic ovary syndrome (PCOS) is characterized by oxidative stress (OS). This study reveals a novel epigenetic mechanism linking lysine acetyltransferase 5 (KAT5) and thrombospondin-1 (TSP-1) in PCOS pathogenesis. A meta-analysis of 50 clinical studies demonstrated elevated systemic oxidative markers (total oxidant status, nitric oxide, malondialdehyde) and reduced paraoxonase-1 levels in PCOS patients, alongside compromised total antioxidant capacity in follicular fluid. Bioinformatic analysis identified TSP-1 as a key downregulated gene in PCOS, and the hTFtarget database predicted KAT5 as an upstream regulator of TSP-1. In vitro, H₂O₂-induced oxidative stress in KGN granulosa cells suppressed TSP-1, KAT5, and H2AK5ac levels, which were restored by N-acetylcysteine (NAC). Mechanistically, KAT5 was found to regulate TSP-1 expression via H2AK5 acetylation at its promoter. Knockdown of KAT5 exacerbated oxidative stress, apoptosis, and senescence, while TSP-1 overexpression counteracted these effects. In a letrozole-induced PCOS rat model, ovarian tissues exhibited decreased H2AK5 acetylation, reduced KAT5 and TSP-1 expression, and impaired redox homeostasis. Interventions with N-acetylcysteine or TSP-1 ameliorated ovarian pathological changes, hormonal imbalances, oxidative stress, apoptosis, and cellular senescence. Collectively, these findings establish the KAT5-TSP-1 axis as a critical regulator of ovarian redox homeostasis, unveiling a novel epigenetic mechanism and proposing a dual-target therapeutic strategy for PCOS.</p>","PeriodicalId":20920,"journal":{"name":"Reproductive Sciences","volume":" ","pages":"1838-1857"},"PeriodicalIF":2.8,"publicationDate":"2026-09-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"148550269","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":3,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Obeticholic Acid Rescues Male Reproductive Function in High-Fat Diet-Induced Metabolic Syndrome.","authors":"Jin-Chuan Liu, Qunxiong Zeng, Dongliang Li, Tianyi Ma, William S B Yeung, Tao Zhang, Yong-Gang Duan","doi":"10.1007/s43032-026-02180-x","DOIUrl":"https://doi.org/10.1007/s43032-026-02180-x","url":null,"abstract":"<p><p>Metabolic syndrome (MetS) contributes to male infertility, yet the impact of MetS-targeted therapies on fertility remains unclear. This study investigates the impact of obeticholic acid (OCA), a farnesoid X receptor (FXR) agonist, in a high-fat-diet (HFD)-induced MetS mouse model. MetS was induced in male mice by 12-week of HFD feeding. Mice then received OCA (30 mg/kg) or vehicle for 5 weeks. Sperm parameters, testicular and epididymal immune profiles, intestinal bile acid, gut microbiota, and epididymal gene expression were assessed. OCA treatment was associated with higher sperm progressive motility (PR) and lower proportions of epididymal IFN-γ-producing CD4⁺ T helper 1 (Th1) cells. OCA shifted bile acid profile and gut microbiota. Expression of H2bc24 in epididymis increased to levels comparable with control group. These findings indicate that OCA is associated with improved male reproductive parameters in MetS through modulation of bile acid signaling, immune response, and microbiota. OCA may represent a potential therapeutic approach for MetS- associated male infertility.</p>","PeriodicalId":20920,"journal":{"name":"Reproductive Sciences","volume":" ","pages":""},"PeriodicalIF":2.8,"publicationDate":"2026-09-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"148874834","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":3,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Weighted Gene Co-Expression Network Analysis and Machine Learning Reveal that USP1 Drives Lipid Metabolism and Macrophage Polarization in Cervical Cancer Cells.","authors":"Xiaojuan Wang, Fang Wang, Wenjing Yang, Yunxia Li","doi":"10.1007/s43032-026-02172-x","DOIUrl":"10.1007/s43032-026-02172-x","url":null,"abstract":"<p><p>Cervical cancer is a leading preventable cause of cancer morbidity and mortality globally. Previous studies have indicated that dysregulation of the ubiquitin-proteasome system participates in lipid metabolism and cervical cancer progression. However, the role and mechanism of deubiquitinase ubiquitin-specific protease 1 (USP1) in cervical cancer are still unclear. The cervical cancer transcriptome data from the GSE90738 database were downloaded from the Gene Expression Omnibus dataset. Differential expression gene (DEG) analysis, weighted gene coexpression network analysis (WGCNA), GeneCards database, and ubibrowser2.0 database were employed to identify potential ubiquitin-related targets involved in lipid metabolism during cervical cancer progression. Then, these intersected targets were subjected to cross-validation using three machine learning algorithms-Least Absolute Shrinkage and Selection Operator (LASSO) regression, Support Vector Machine Recursive Feature Elimination (SVM-RFE), and Random Forest (RF), ultimately identifying one hub gene. GSE90738 and GEPIA databases were used to analyze USP1 expression in cervical cancer patients. The relationship between USP1 and overall survival or progress-free survival of cervical cancer patients was analyzed. USP1 mRNA level was detected by real-time quantitative polymerase chain reaction (RT-qPCR). USP1, FASN, and GPX4 protein levels were determined using western blot assay. Cell proliferation was detected using 5-ethynyl-2'-deoxyuridine (EdU) and colony formation assays. Lipid accumulation (Oil Red O/Nile Red), lipid-ROS, and ferrous iron levels were measured using special kits. A co-culture model of THP1 macrophages and cervical cancer cells was conducted to investigate the impacts of tumor cell-derived USP1 on THP1 macrophage polarization. The effect of USP1 on tumorigenesis was examined using a xenograft tumor model in vivo. A total of 19 potential signature genes were identified by DEG analysis, WGCNA, GeneCards database, and ubibrowser2.0 database. Through the three machine learning algorithms of LASSO, RF, and SVM-RFE, one hub gene (USP1) was identified with diagnostic potential. Furthermore, USP1 was upregulated in cervical cancer, and its silencing could repress cervical cancer cell proliferation, lipid metabolism, and promote ferroptosis. Meanwhile, USP1 silencing could hinder M2 polarization of TAMs by downregulating TGF-β1 and IL-10. Besides, USP1 deficiency suppressed tumor growth in vivo. Through bioinformatics analysis and experiments, this study discovered that USP1 knockdown inhibited cervical cancer growth and TAM M2 polarization, providing a promising therapeutic target for cervical cancer treatment.</p>","PeriodicalId":20920,"journal":{"name":"Reproductive Sciences","volume":" ","pages":"1760-1774"},"PeriodicalIF":2.8,"publicationDate":"2026-09-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"148814032","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":3,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Association of GPR30 Genetic Variants with Recurrent Implantation Failure: A Case-Control Study Comparing Fertile Women, ART Success and RIF Patients.","authors":"Elham Khatibi, Fatemeh Saeedi, Parnaz Borjian Boroujeni, Mehri Mashayekhi, Azadeh Ghaheri, Mohammadreza Zamanian","doi":"10.1007/s43032-026-02178-5","DOIUrl":"10.1007/s43032-026-02178-5","url":null,"abstract":"<p><p>GPR30 (G-protein coupled receptor 30) plays a key role in regulating reproductive processes, particularly through estrogen signaling. Previous studies have linked GPR30 polymorphisms to female reproductive disorders such as infertility, recurrent pregnancy loss, endometriosis, leiomyoma, and breast or ovarian cancers. This study investigated, for the first time, the association between two GPR30 polymorphisms (rs3808350 and rs3808351) and recurrent implantation failure (RIF) in infertile women referred to the Royan Institute. A total of 300 Iranian women were divided into three groups: 100 with RIF, 100 fertile controls, and 100 women with successful ART outcomes as a second control group. The frequencies of rs3808350 and rs3808351 polymorphisms were analyzed using ARMS-PCR, and confirmed by Sanger sequencing. Statistical analysis was performed using Chi-square and Fisher's exact tests (p ≤ 0.05). For rs3808350, genotype frequencies significantly differed across the three groups (p < 0.001), though allele frequencies did not (p = 0.107). Further comparison between the RIF and ART+ groups showed significant differences in both genotype (p = 0.005) and allele (p = 0.041) frequencies. For rs3808351, significant differences in both genotype and allele frequencies were observed among all groups (p < 0.001). These findings suggest that rs3808350 and rs3808351 polymorphisms in the GPR30 gene are significantly associated with increased risk of recurrent implantation failure.</p>","PeriodicalId":20920,"journal":{"name":"Reproductive Sciences","volume":" ","pages":"1858-1866"},"PeriodicalIF":2.8,"publicationDate":"2026-09-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"148797614","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":3,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Polyendocrine Metabolic Ovarian Syndrome (PMOS; Formerly Polycystic Ovary Syndrome/PCOS) and Susceptibility to Microbial Infections: Mechanisms, Clinical Management, and Reproductive Consequences - A Comprehensive Review.","authors":"Ali Samareh, Mohammad Samare-Najaf, Mehrangiz Ghafari, Hossein Pourghadamyari, Gholamreza Asadikaram, Morteza Barkam, Sanaz Rastegar","doi":"10.1007/s43032-026-02176-7","DOIUrl":"10.1007/s43032-026-02176-7","url":null,"abstract":"<p><p>Polyendocrine metabolic ovarian syndrome (PMOS), formerly known as polycystic ovary syndrome (PCOS), is a common endocrine-metabolic disorder characterized by hyperandrogenism, insulin resistance, ovulatory dysfunction, and chronic low-grade inflammation. Recent studies suggest that PMOS may also be associated with altered immune regulation and changes in the gut and vaginal microbiomes. This review summarizes current evidence on the possible relationship between PMOS and susceptibility to microbial infections, with emphasis on mechanisms, clinical management, and reproductive consequences. A narrative review of mechanistic, clinical, epidemiological, and microbiome studies was conducted to evaluate how PMOS-related endocrine, metabolic, inflammatory, and microbial changes may influence infection risk and reproductive outcomes. Available evidence suggests that women with PMOS may be more vulnerable to selected infection-related conditions, especially vaginal dysbiosis, bacterial vaginosis, and vulvovaginal candidiasis. Proposed mechanisms include insulin resistance, hyperandrogenism, chronic inflammation, altered immune cell activity, impaired mucosal defense, and reduced Lactobacillus dominance. Evidence for urinary tract infections, systemic bacterial infections, and viral infections is less consistent and is often affected by confounding factors such as obesity and metabolic disease. PMOS may involve altered immune and microbiome regulation rather than generalized immunosuppression. Clinical care should focus on established PMOS management, metabolic optimization, risk-based infection evaluation, and treatment of confirmed infections. Microbiome-targeted therapies remain investigational until supported by stronger PMOS-specific evidence.</p>","PeriodicalId":20920,"journal":{"name":"Reproductive Sciences","volume":" ","pages":"1816-1837"},"PeriodicalIF":2.8,"publicationDate":"2026-09-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"148819485","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":3,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Identification of a Novel Splice-Site variant in TACR3 (c.888 + 1G > A) Associated with Asthenozoospermia and Hypogonadotropic Hypogonadism in an Iranian Family.","authors":"Mohammadreza Saberiyan, S M Kalantar, Reza Mirfakhraie, Hossein Teimori, Naser Riazi, Azim Nejatizadeh","doi":"10.1007/s43032-026-02131-6","DOIUrl":"10.1007/s43032-026-02131-6","url":null,"abstract":"<p><strong>Background: </strong>TACR3 encodes the receptor for neurokinin B, a key regulator of the hypothalamic-pituitary-gonadal axis. Disruption of this pathway can impair gonadotropin release and male reproductive function. Given the genetic heterogeneity of male infertility, this study aimed to identify novel variants in TACR3 that may underlie asthenozoospermia and related hormonal abnormalities.</p><p><strong>Methods: </strong>Fifteen infertile men with confirmed asthenozoospermia were enrolled. Whole-exome sequencing (WES) was performed on genomic DNA from peripheral blood, and the candidate variant was validated by Sanger sequencing. Functional predictions were made using PolyPhen-2, SIFT, MutationTaster, and REVEL. TACR3 mRNA expression levels were assessed by real-time PCR in available samples.</p><p><strong>Results: </strong>A novel splice-site variant, TACR3 (NM_001059.3:c.888 + 1G > A), was detected and found to segregate with infertility in one family, appearing homozygously in two infertile brothers and heterozygously in the proband with severe asthenozoospermia. The variant was absent in public and local genomic databases, suggesting its extremely rare frequency. Furthermore, RT-PCR showed a dramatic reduction or complete loss of TACR3 expression in affected individuals, confirming its deleterious effect on splicing and mRNA stability.</p><p><strong>Conclusion: </strong>We identified a previously unreported splice-site mutation in TACR3 (c.888 + 1G > A) that likely causes familial infertility by disrupting the neurokinin B/NK3R signaling pathway. While the heterozygous proband exhibited severe asthenozoospermia, the homozygous brothers displayed hormonal profiles typical of hypogonadotropic hypogonadism. These findings extend the mutational landscape of TACR3 and highlight its essential contribution to male reproductive endocrinology.</p>","PeriodicalId":20920,"journal":{"name":"Reproductive Sciences","volume":" ","pages":"1705-1713"},"PeriodicalIF":2.8,"publicationDate":"2026-09-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"148606903","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":3,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Smartphone-Assisted CSCTAS-Derived Sperm Kinematics and Clinical Pregnancy after Intrauterine Insemination in a Turkish Cohort of Couples with Unexplained Infertility.","authors":"Esra Selvi, Ayşe Altun Akpınar, Yeşim Erkan, Hamza Osman İlhan, Nizamettin Aydın, Özlem Dural, Necip Erkut Attar","doi":"10.1007/s43032-026-02165-w","DOIUrl":"10.1007/s43032-026-02165-w","url":null,"abstract":"<p><p>Conventional semen analysis provides limited information on sperm kinematic behavior in couples with unexplained infertility undergoing intrauterine insemination (IUI). We used a laboratory based, microscope mounted smartphone-assisted Computerized Sperm Counting and Tracking Analysis System (CSCTAS) to characterize sperm kinematics in prepared samples and compare them by ultrasound-confirmed clinical pregnancy after IUI. In this retrospective single-center Turkish cohort, 184 first IUI cycles between January 2018 and December 2019 were analyzed. Prepared samples were assessed under standardized Makler chamber conditions. Manual-CSCTAS agreement for total motility was assessed by Bland-Altman analysis, and single-variable receiver operating characteristic analyses were supplementary. Clinical pregnancy occurred in 29 cycles (15.8%). Pre- and post-preparation semen parameters were similar between groups. Mean CSCTAS-derived wobble (WOB) was higher in pregnancy-positive cycles (0.83 ± 0.03 vs. 0.81 ± 0.09; p = 0.004; Cohen's d = 0.24), whereas beat-cross frequency (BCF) was lower at the nominal level (7.28 ± 0.70 vs. 7.61 ± 1.05 Hz; p = 0.039; d = - 0.33). Although statistically significant, the differences had small effect sizes. Bland-Altman analysis showed a mean bias of - 3.44% points, 95% limits of agreement of - 24.69 to 17.81, and proportional bias. Single-variable area under the curve (AUC) values were 0.526 for WOB and 0.555 for BCF, and both 95% confidence intervals included 0.50. These findings suggest exploratory population-level digital motility signals; however, the small effect sizes and near-chance single-variable AUC values indicate limited predictive performance and do not support their use as standalone predictors of individual IUI outcome.</p>","PeriodicalId":20920,"journal":{"name":"Reproductive Sciences","volume":" ","pages":"1687-1699"},"PeriodicalIF":2.8,"publicationDate":"2026-09-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"148562897","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":3,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Endometrial Repair and Regenerative Medicine: From Broad-Spectrum Regeneration to Precision Intervention.","authors":"Mengqi Xie, Yungui Cao, Jiangping Tang, Fang Li, Juan Deng","doi":"10.1007/s43032-026-02150-3","DOIUrl":"10.1007/s43032-026-02150-3","url":null,"abstract":"&lt;p&gt;&lt;p&gt;Endometrial injury-related disorders, including intrauterine adhesions, thin endometrium, and chronic endometritis, are a major cause of female infertility. Conventional therapeutic approaches, primarily hormone therapy and surgical interventions, show limited effectiveness in patients with moderate to severe endometrial damage. In this context, regenerative medicine has emerged as a promising direction to overcome current therapeutic limitations and promote functional reconstruction of the endometrium. A comprehensive literature search was conducted across PubMed, Web of Science, Embase, and Scopus to identify relevant studies on endometrial repair and regenerative medicine. The search covered publications from January 2000 to August 2025. The following keyword combinations and MeSH terms were used: (\"endometrial repair\" OR \"endometrial regeneration\" OR \"intrauterine adhesion\" OR \"Asherman syndrome\" OR \"thin endometrium\" OR \"chronic endometritis\") AND (\"mesenchymal stem cells\" OR \"platelet-rich plasma\" OR \"exosomes\" OR \"extracellular vesicles\" OR \"biomaterials\" OR \"hydrogel\" OR \"scaffold\" OR \"regenerative medicine\"). Both basic science investigations and clinical studies were included to provide a comprehensive overview of current developments in the field. To minimize the risk of omission, the reference lists of included articles and relevant reviews were manually screened, and potentially pertinent studies were further evaluated. Inclusion criteria: (1) Original research articles or meta-analyses; (2) Focus on therapeutic interventions for endometrial regeneration; (3) Human clinical studies or mammalian animal models. Exclusion criteria: (1) Non-English articles, letters, conference proceedings, etc.; (2) Purely descriptive studies of endometrial physiology without therapeutic intervention, articles lacking quantitative data or sufficient methodological details. The screening process followed the PRISMA 2020 guidelines (Fig. 1). After removing duplicates, 1936 records were screened by title and abstract, and 605 full-text articles were assessed for eligibility. Finally, 102 studies were included in this qualitative synthesis. This review provides a systematic synthesis of recent advances in cell-based therapies, cell-free approaches, and bioengineering strategies for endometrial repair. Evidence derived from different sources of mesenchymal stem cells, including bone marrow, umbilical cord, and endometrium, is comparatively evaluated alongside platelet-rich plasma and extracellular vesicles, with an emphasis on hierarchical assessment of evidence levels. Several critical issues are further examined. Current stem cell-based interventions are largely characterized by a broad reparative profile, yet precise targeting of key molecular mechanisms remains insufficient. To date, no studies have demonstrated the capacity to directly reverse suppression of signaling pathways such as the GZMA-PARD3 axis or to restore depleted regenerative stromal","PeriodicalId":20920,"journal":{"name":"Reproductive Sciences","volume":" ","pages":"1867-1889"},"PeriodicalIF":2.8,"publicationDate":"2026-09-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC13562326/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"148606910","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":3,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Effects of Acute Hypoxic Exposure on Ovarian Function in Female Mice.","authors":"Jimei Li, Shuqiang Chen, Ruiping Bai, Lu Wang, Ranran Lang, Ying Ju","doi":"10.1007/s43032-026-02167-8","DOIUrl":"10.1007/s43032-026-02167-8","url":null,"abstract":"<p><p>To investigate the effects of acute high-altitude hypoxia on ovarian function and ovarian tissue transcriptomics in female mice, providing experimental evidence for elucidating the mechanisms underlying female reproductive damage caused by acute high-altitude hypoxia. Sixty female mice were randomized into three groups (20 mice each): control (CON, 500 m, conventional housing for 14 d), 7 d hypoxic exposure (LO1) and 14 d hypoxic exposure (LO2). LO1 and LO2 were kept in a low-pressure hypoxic chamber simulating 5500 m. Serum reproductive hormones (AMH, FSH, LH, E₂) and oxidative stress markers were detected; ovarian indices were calculated and ovarian histopathology examined. Additionally, transcriptome sequencing and functional enrichment analysis of differentially expressed genes were conducted on ovarian tissues. Compared with CON, LO1 and LO2 showed markedly decreased serum AMH, LH and E₂ (P < 0.01), sharply elevated FSH (P < 0.001), increased malondialdehyde (P < 0.001), reduced superoxide dismutase activity (P < 0.01), first increased then decreased total antioxidant capacity (P < 0.001), and lower ovarian index (P < 0.01). Histology showed ovarian atrophy and ischemic congestion, with fewer primary, secondary and mature follicles (P < 0.05) and more atretic follicles in LO2 (P < 0.05). Transcriptome sequencing found 234 significantly differentially expressed genes, whose co-differentially expressed ones were enriched in oxygen transport/oxidative stress and steroid hormone synthesis pathways. Acute high-altitude hypoxia impairs ovarian reserve function and disrupts follicular development in female mice, potentially through oxidative stress imbalance and dysregulation of genes involved in steroid hormone synthesis pathways.</p>","PeriodicalId":20920,"journal":{"name":"Reproductive Sciences","volume":" ","pages":"1783-1793"},"PeriodicalIF":2.8,"publicationDate":"2026-09-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"148621314","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":3,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Circulating Cardiovascular Biomarkers 1-3 Years Following Hypertensive Pregnancy Disorders: Associations With Postpartum Cardiovascular Structure and Function.","authors":"Kristina Klepp, Kjartan Moe, Daniel P Jacobsen, Meryam Sugulle, Kristin Angel, Thomas G von Lueder, Ralf Dechend, Anne Cathrine Staff","doi":"10.1007/s43032-026-02171-y","DOIUrl":"10.1007/s43032-026-02171-y","url":null,"abstract":"<p><p>Hypertensive disorders of pregnancy (HDP) confer increased cardiovascular disease (CVD) risk postpartum. Screening methods targeting women with increased risk are lacking, limiting personalized follow-up. Circulating biomarkers may assist CVD risk stratification. We aimed to assess whether circulating biomarkers were associated with measures of cardiovascular structure and function following HDP and normotensive pregnancies (controls). We examined 275 women 1-3 years postpartum (176 following HDP and 99 parous controls). Circulating biomarkers (hs-CRP, non-HDL cholesterol, glucose, eGFR, cTnT, NT-proBNP, GDF-15, sHLA-G, SAA1) and cardiovascular function and structure measures were examined [pulse wave velocity (PWV), carotid intima-media thickness (CIMT) and echocardiography]. Group differences were tested by Mann-Whitney U test and chi-square. Associations were assessed by univariate regression analyses. A p-value < 0.05 was considered statistically significant. Women following HDP displayed significantly higher rates of hypertension (5% vs. 0%) and metabolic syndrome (7% vs. 1%) than controls. Circulating biomarker levels were similar between study groups. In univariate regression analyses for the prior HDP group, non-HDL cholesterol was significantly associated with PWV and CIMT. Additionally, glucose and hs-CRP were significantly associated with PWV. These associations were not reproduced for controls, except for non-HDL cholesterol which was significantly associated with CIMT. In conclusion, women following HDP and normotensive pregnancies had similar postpartum levels of circulating biomarkers, but circulating biomarkers were significantly associated with measures of arterial stiffness (PWV and CIMT) in women with prior HDP. Our findings support current guidelines recommending CVD follow-up after HDP. Non-HDL cholesterol, glucose and hs-CRP may possibly help refining personalized cardiovascular follow-up postpartum.</p>","PeriodicalId":20920,"journal":{"name":"Reproductive Sciences","volume":" ","pages":"1659-1673"},"PeriodicalIF":2.8,"publicationDate":"2026-09-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC13562120/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"148797626","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":3,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}