Journal of Ovarian Research最新文献

{"title":"Exploring causal relationships between brain imaging-derived phenotypes and ovarian cancer risk: a bidirectional Mendelian randomization.","authors":"Ting Liu, Xiaoqian Tuo, Huifang Zhao, Yan Wang, Yu Jiang, Jiaojiao Lu","doi":"10.1186/s13048-025-01733-z","DOIUrl":"https://doi.org/10.1186/s13048-025-01733-z","url":null,"abstract":"<p><strong>Background: </strong>Ovarian cancer could induce alterations in both structure and function of the brain. This study employs Mendelian randomization (MR) to investigate the causal relationship between brain imaging-derived phenotypes (IDPs) and ovarian cancer, offering new insights into the potential clinical applications of IDPs for ovarian cancer risk assessment.</p><p><strong>Methods: </strong>This study identified 587 brain IDPs using structural and diffusion magnetic resonance imaging (MRI) data from the UK Biobank and data were sourced from two independent Genome-Wide Association Studies (GWAS). We selected single nucleotide polymorphisms (SNPs) as instrumental variables based on rigorous criteria. To evaluate the causal effects of IDPs on the risk of ovarian cancer, we employed five MR models: Inverse Variance Weighted (IVW), MR-Egger regression, Weighted median, Weighted mode, and Simple mode. Furthermore, we conducted a meta-analysis to provide additional validation for our results.</p><p><strong>Results: </strong>Forward MR analysis identified 72 IDPs that were significantly associated with the risk of ovarian cancer, with 65 remaining robust after conducting sensitivity tests. Conversely, reverse MR analysis indicated that 63 IDPs were influenced by ovarian cancer, highlighting a bidirectional causal relationship between these factors. The meta-analysis revealed that an increased cortical surface area of the right precentral gyrus was associated with a heightened risk of ovarian cancer, with an odds ratio (OR) of 1.139 (95% confidence interval [CI]: 1.037-1.250, P = 0.006, common effect model). In contrast, a larger volume of the right medial orbital frontal cortex was linked to a reduced risk of ovarian cancer, with an OR of 0.839 (95% CI: 0.744-0.946, P = 0.004, common effect model). Additionally, in the reverse MR analysis, a higher risk of ovarian cancer was associated with an increased fractional anisotropy (FA) in the right fornix and stria terminalis, while decreased orientation dispersion index (OD) in the left anterior corona radiata.</p><p><strong>Conclusions: </strong>This study provides compelling evidence of a causal relationship between IDPs and ovarian cancer risk. It suggests that IDPs might serve as valuable biomarkers for ovarian cancer risk assessment at brain-imaging levels and emphasize the need for further research to explore the biological mechanisms underlying these associations.</p>","PeriodicalId":16610,"journal":{"name":"Journal of Ovarian Research","volume":"18 1","pages":"173"},"PeriodicalIF":4.2,"publicationDate":"2025-08-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144765007","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":"Mechanisms of cell senescence and apoptosis in cyclophosphamide-induced premature ovarian failure in rats.","authors":"Jiaqi Wu, Yanmeng Wei, Qiangli Peng, Jing Zhu, Huacong Shi, Ting Zhao, Tao Yuan","doi":"10.1186/s13048-025-01759-3","DOIUrl":"https://doi.org/10.1186/s13048-025-01759-3","url":null,"abstract":"<p><strong>Background: </strong>Premature ovarian failure (POF) is a clinical condition characterized by a diminished ovarian reserve occurring before the age of 40, significantly affecting female reproductive health. However, its exact pathogenesis remains unclear. This research aimed to examine the mechanisms of cyclophosphamide (CTX)-induced senescence and apoptosis in the ovarian and cerebral cortex tissues of rats to provide insights into delaying aging and protecting female reproductive health.</p><p><strong>Methods: </strong>A rat model of POF was established by intraperitoneal injection of CTX. Model efficacy was evaluated by measuring ovarian volume, weight, estrogen, and anti-Müllerian hormone levels. Serum marker changes were detected via enzyme-linked immunosorbent assay (ELISA). Senescence and apoptosis in cerebral cortical and ovarian tissues were observed using β-galactosidase (SA-β-gal) staining and terminal deoxynucleotidyl transferase dUTP nick-end labeling (TUNEL) assay. Western Blot and quantitative polymerase chain reaction (RT-qPCR) were employed to detect the expression levels of cell senescence- and apoptosis-related proteins and genes, verifying the correlation between POF and cellular senescence/apoptosis.</p><p><strong>Results: </strong>High-dose CTX induced POF. In rats with POF, the levels of anti-Müllerian hormone (AMH), estradiol (E2), and vitamin D (VD) significantly decreased (P < 0.0001), whereas the levels of testosterone (T) and insulin (INS) significantly increased (P < 0.0001). The number of senescent and apoptotic-positive cells in the ovarian and cerebral cortex tissues of rats with POF was substantially augmented (P < 0.05; P < 0.01). Additionally, the expression of senescence-related proteins cyclin-dependent kinase inhibitor 1 A (CDKN1A), cyclin-dependent kinase inhibitor 2 A (CDKN2A), tumor protein p53 (P53), apoptosis-related protein BCL2-Associated X Protein (Bax), and cysteine-aspartic acid protease 3 (caspase 3) was upregulated. In contrast, the expression of the anti-apoptotic protein BCL-2 was downregulated. The changes ranged from 1.7- to 7.1-fold. These findings demonstrated that high-dose CTX injection leads to cellular senescence and apoptosis, resulting in ovarian pathology.</p><p><strong>Conclusion: </strong>High-dose CTX induced POF in rats, resulting in aging and apoptosis in the cerebral cortex and ovarian tissues. Therefore, inhibiting cellular senescence and apoptosis may be a potential approach for restoring ovarian reserve function in POF.</p>","PeriodicalId":16610,"journal":{"name":"Journal of Ovarian Research","volume":"18 1","pages":"172"},"PeriodicalIF":4.2,"publicationDate":"2025-07-31","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144760294","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":"Premature ovarian insufficiency restoration after chemotherapy: current achievements and future prospects on its treatment or management.","authors":"Hamideh Aboutalebi, Shayan Vafaei, Mohammad Aboutalebi, Hengameh Dortaj, Fatemeh Alipour, Alireza Ebrahimzadeh- Bideskan","doi":"10.1186/s13048-025-01677-4","DOIUrl":"10.1186/s13048-025-01677-4","url":null,"abstract":"<p><p>One of the important discussions in assisted reproductive technology (ART) is to maintain fertility in those who are at risk of losing their fertility for various reasons, including cancer and the use of anti-cancer therapies, hence finding a way to maintain fertility during chemotherapy, is vital. Nowadays, in addition to successfully treating patients, oncologists have also focused their attention on preserving their patients' potential of the latter to conceive. Chemotherapy-related ovarian failure, which manifests as a non-physiological form of amenorrhea, can cause dysfunction of the ovary. It is hypothesized that chemotherapeutic agents may cause DNA damage, accelerate follicular apoptosis, oxidative stress, resulting in loss of ovarian reserve function. Hence investigation on utilization of alternatives in order to maintain ovarian function and fertility in cancer survivors seems important. This review provides an update on available and potential future prospects for fertility preservation in women treated with chemotherapy.</p>","PeriodicalId":16610,"journal":{"name":"Journal of Ovarian Research","volume":"18 1","pages":"171"},"PeriodicalIF":4.2,"publicationDate":"2025-07-31","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC12312501/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144760295","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":"Hyperandrogenism-mediated YAP activation drives ovarian inflammation and pyroptosis in PCOS: implications for follicular dysfunction.","authors":"Tianyue Xu, Yu Xiang, Zichao Huang, Qi Zhu, Honghui Wu, Jieyu Cai, Linglin Weng, Hongshan Ge","doi":"10.1186/s13048-025-01757-5","DOIUrl":"10.1186/s13048-025-01757-5","url":null,"abstract":"<p><strong>Background: </strong>Hyperandrogenism and persistent chronic inflammation significantly contribute to ovarian dysfunction in polycystic ovary syndrome (PCOS). Although the exact connection between hyperandrogenism and inflammation in PCOS remains unclear, the Hippo pathway, also seems to be involved in the inflammatory response through YAP.</p><p><strong>Method: </strong>An in-vivo PCOS model of mice was constructed with dehydroepiandrosterone (DHEA) and YAP inhibitor Verteporfin (VP). YAP, inflammation and pyroptosis levels of ovarian tissues were detected in mice models. An in-vitro PCOS model of KGN cells was constructed with testosterone, and YAP was knocked down by lentivirus.</p><p><strong>Results: </strong>Increased levels of YAP in the ovarian tissues of the DHEA-treated mice were observed, alongside elevations in inflammation and pyroptosis levels, whereas Verteporfin reversed these alterations. The findings in KGN cells demonstrated that testosterone treatment results in elevation of YAP, inflammation and pyroptosis levels in granulosa cells. However, knocking down YAP in KGN cells curtailed testosterone-induced inflammation and pyroptosis.</p><p><strong>Conclusions: </strong>Hyperandrogenism in PCOS promotes ovarian inflammation by upregulating nuclear YAP, disrupting the inflammatory microenvironment, leading to abnormal ovarian pyroptosis, and ultimately impairing follicular function.</p>","PeriodicalId":16610,"journal":{"name":"Journal of Ovarian Research","volume":"18 1","pages":"170"},"PeriodicalIF":4.2,"publicationDate":"2025-07-30","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC12312577/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144753593","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":"Notch2 improves granulosa cell functions in premature ovarian failure by activating the Wnt2/β-catenin pathway.","authors":"Xia Liang, Nina Li, Senyan Wu","doi":"10.1186/s13048-025-01745-9","DOIUrl":"10.1186/s13048-025-01745-9","url":null,"abstract":"<p><strong>Background: </strong>Notch2 and Wnt2/β-catenin pathway improve granulosa cell (GC) functions, and there are interactions between Notch and Wnt/β-catenin in some cells. We aimed to investigate whether Notch2 improves GC functions in premature ovarian failure (POF) by activating the Wnt2/β-catenin pathway.</p><p><strong>Methods: </strong>Notch2 expression was interfered in mice or KGN cells, then, mice were treated with cyclophosphamide and busulfan intraperitoneally, and KGN cells were exposed to cyclophosphamide to establish POF models. In vivo, the number of follicles at different stages was counted, and interactions between Notch2 and Wnt2 were detected. In vitro, cell viability and cycle were measured. Additionally, hormone levels, oxidative stress (OS) degrees, cell apoptosis, Notch2 and Wnt2/β-catenin pathway-related genes were detected in vivo and in vitro. Finally, Wnt/β-catenin pathway inhibitor (IWR-1), agonist (SKL2001) and β-catenin knockdown were used.</p><p><strong>Results: </strong>Notch2 overexpression not only improved hormone levels, follicular development, OS degree and ovarian cell apoptosis, but also activated Wnt2/β-catenin pathway for POF mice. Moreover, Notch2 interacted with Wnt2 in POF mice. In vitro, Notch2 knockdown decreased cell viability, disrupted cell cycle, increased cell apoptosis, worsened hormone levels, promoted OS degree and inhibited Wnt2/β-catenin pathway for POF. Importantly, the protective effects of Notch2 overexpression and the worsening impacts of Notch2 knockdown on POF were reversed by IWR-1 and SKL2001. β-Catenin knockdown further impaired GC functions in POF models that underwent Notch2 and β-catenin knockdown.</p><p><strong>Conclusion: </strong>Notch2 may improve GC functions in POF by activating the Wnt2/β-catenin pathway, suggesting that the Notch2-mediated Wnt2/β-catenin pathway is a novel therapeutic target for POF.</p>","PeriodicalId":16610,"journal":{"name":"Journal of Ovarian Research","volume":"18 1","pages":"169"},"PeriodicalIF":4.2,"publicationDate":"2025-07-30","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC12308925/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144753594","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":"Mechanism by which SUGT1 downregulates FH to promote proliferation and migration in serous ovarian cancer.","authors":"Tianli Mu, Bo Ren, Ziteng Kuang, Runze He, Bingjie Rui, Ye Yang, Yuxi Liu, Danbo Geng, Yuci Zhang, Min Wang","doi":"10.1186/s13048-025-01744-w","DOIUrl":"10.1186/s13048-025-01744-w","url":null,"abstract":"<p><strong>Background: </strong>SUGT1 (Suppressor of the G2 allele of SKP1) and FH (fumarate hydratase) have recently garnered significant attention from the research community. SUGT1 functions as a molecular chaperone, regulating the stability and activity of various proteins, while FH is a key enzyme in the tricarboxylic acid cycle, catalyzing the reversible conversion of fumarate to malate. Existing literature has established their essential roles in signaling, tumorigenesis, and cancer progression. However, their functions and mechanisms in ovarian cancer (OC) remain poorly understood.</p><p><strong>Results: </strong>We found that high SUGT1 expression is associated with a more advanced FIGO stage in OC. SUGT1 knockdown significantly inhibits OC cell proliferation and metastasis, while its overexpression has the opposite oncogenic effect. Mechanistically, we revealed that SUGT1 promotes FH protein degradation via the ubiquitin-proteasome pathway. Moreover, FH knockdown partly reversed the inhibitory effects of SUGT1 knockdown on tumor cell proliferation, migration, and proteins of phosphorylated PI3K/AKT and Vimentin. In summary, We demonstrated that SUGT1 exerts oncogenic functions in OC by regulating FH stability.</p><p><strong>Conclusions: </strong>Our study is the first to provide experimental evidence elucidating the SUGT1-FH relation and its role in OC progression, offering potential significance for clinical diagnosis and therapy.</p>","PeriodicalId":16610,"journal":{"name":"Journal of Ovarian Research","volume":"18 1","pages":"168"},"PeriodicalIF":4.2,"publicationDate":"2025-07-29","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC12309033/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144742360","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":"The role of ultrasound-guided tru-cut biopsy in ovarian cancer: a systematic review of its safety, adequacy, and accuracy with meta-analysis of diagnostic performance.","authors":"Munachiso Iheme Ndukwe, Matteo Pavone, Dominik Habes, Nicolo Bizzarri, Martin Stepan, Petra Bretová, Floriana Mascilini, Dominik Karasek, Denisa Pohankova, Akaninyene Ubom, Jana Marie Havigerova, Jiri Haviger, Igor Sirak","doi":"10.1186/s13048-025-01739-7","DOIUrl":"10.1186/s13048-025-01739-7","url":null,"abstract":"<p><strong>Objectives: </strong>To analyze the safety, adequacy and accuracy of ultrasound-guided tru-cut biopsy in the diagnosis of ovarian cancer.</p><p><strong>Methods: </strong>A systematic search of PubMed, Web of Science, and Scopus was conducted through June 2024. Studies meeting predefined criteria were included in the review. The quality of diagnostic accuracy studies was assessed using QUADAS-2. A meta-analysis was performed on studies reporting complete 2 × 2 diagnostic data.</p><p><strong>Results: </strong>A total of 2,250 articles were initially screened, and after the removal of duplicates, 54 articles were deemed eligible for full-text assessment. Ultimately, 18 studies, comprising 1,867 patients who underwent ultrasound-guided tru-cut biopsy, were included in the systematic review. A total of 16 complications were reported across 1,898 biopsies performed in the included studies, resulting in a mean complication rate of 0.58% (95% CI: 0.187- 0.964%). Adequacy for histological and immunohistochemical examination after one attempt was reported in 16 studies, with a mean adequacy rate of 95.1% (95% CI: 92.69- 97.50%) and a median rate of 95.97%. Diagnostic accuracy was assessed in 13 studies, revealing a mean diagnostic accuracy of 95.54% (95% CI: 93.19- 97.89%) and a median of 97.48%.In the meta-analysis of 10 studies, pooled sensitivity was 98.6%, specificity 41.9%, positive predictive value (PPV) 99.0%, and negative predictive value (NPV) 47.2%, with high heterogeneity observed in specificity and NPV estimates.</p><p><strong>Conclusions: </strong>Ultrasound guided tru-cut biopsy is a safe and effective diagnostic method, demonstrating a high adequacy rate for histological and immunohistochemical analysis. It shows excellent performance in confirming malignancy and supports preoperative decision making. To further define its role in the diagnostic pathway for ovarian cancer, additional prospective multicenter studies are needed-both to validate its reliability in negative cases and to ensure tissue adequacy for advanced molecular testing in the context of personalized medicine.</p>","PeriodicalId":16610,"journal":{"name":"Journal of Ovarian Research","volume":"18 1","pages":"166"},"PeriodicalIF":4.2,"publicationDate":"2025-07-29","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC12308927/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144742362","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":"SLC4A11 is a targetable marker correlated with therapeutic responses in ovarian cancer.","authors":"Xin Li, Jia Yuan, Fanchen Wang, Bin Guan, Wencai Guan, Jimin Shi, Qi Lu, Jihong Zhang, Guoxiong Xu","doi":"10.1186/s13048-025-01758-4","DOIUrl":"10.1186/s13048-025-01758-4","url":null,"abstract":"<p><strong>Background: </strong>Solute carrier family 4 member 11 (SLC4A11) is involved in borate homeostasis, metabolism reprogramming, cell growth, and cell adhesion. However, the biological function of SLC4A11 in ovarian cancer (OC) is still unclear. This study explores the anti-tumor and biological activities of SLC4A11 in OC.</p><p><strong>Methods: </strong>The expression and function of SLC4A11 were evaluated in human OC cells and xenograft mice. SLC4A11 expression was evaluated using data from the TCGA-OV, GTEx, and GEO datasets. The genetic status of SLC4A11 was analyzed by the cBioPortal database. The data of expressional abundance, immunochemistry, and immunofluorescence were analyzed through the HPA database. The correlation between SLC4A11 and immune responses was analyzed with the CIBERSORT database, whereas therapeutic responses were analyzed with the CellMiner database.</p><p><strong>Results: </strong>SLC4A11 was found to be highly expressed in OC tissues/cells and had a relationship with an unfavorable prognosis in patients with OC. The overexpressed SLC4A11 promoted OC cell proliferation, migration, and invasion. Reducing SLC4A11 caused the cell cycle arrest at the G0/G1 phase and triggered apoptosis. The in vivo study with a xenographic model revealed that the knockdown of SLC4A11 suppressed tumor growth. Subsequent bioinformatics analyses revealed that SLC4A11 expression was associated with immune responses and therapeutic drug sensitivity.</p><p><strong>Conclusions: </strong>These findings have illustrated the oncogenic role of SLC4A11 in OC. SLC4A11 is overexpressed and is correlated with poor prognosis in OC. SLC4A11 may be a targetable biomarker and has a potential value of application in treating patients with OC.</p>","PeriodicalId":16610,"journal":{"name":"Journal of Ovarian Research","volume":"18 1","pages":"167"},"PeriodicalIF":4.2,"publicationDate":"2025-07-29","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC12309138/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144742361","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":"Ovarian aging, cardiovascular risk and inflammation: insights from the OVA study.","authors":"C Verhaeghe, K J Lindquist, M E Bleil, M Rosen, R F Redberg, D Haisenleder, C E McCulloch, Marcelle I Cedars","doi":"10.1186/s13048-025-01754-8","DOIUrl":"10.1186/s13048-025-01754-8","url":null,"abstract":"<p><strong>Background: </strong>Cardiovascular disease is the leading cause of death among women and is associated with both metabolic syndrome and ovarian aging. Chronic inflammation has been proposed as a potential common underlying mechanism linking these conditions. This study aimed to examine the associations between inflammatory markers (interleukin-6, tumor necrosis factor-alpha, high-sensitivity C-reactive protein) and metabolic syndrome, with markers of ovarian aging and cardiovascular risk.</p><p><strong>Results: </strong>In the cross-sectional analysis of 829 women aged 25-45, no significant associations were found between inflammatory markers, metabolic syndrome, and ovarian aging measures (anti-Müllerian hormone [AMH] and antral follicle count [AFC]), except for a modest association between metabolic syndrome and AMH (mean difference 0.085; 95% CI: 0.035 to 0.134). Similarly, inflammatory markers and metabolic syndrome were not significantly associated with the Framingham Risk Score. In the longitudinal analysis of 307 participants, changes in AMH and AFC were not associated with inflammatory markers or metabolic syndrome. However, higher levels of IL-6 and TNF-α were associated with the Framingham Risk Score, whereas hsCRP and metabolic syndrome were not.</p><p><strong>Conclusion: </strong>These findings do not support the hypothesis that inflammation is a central mechanism linking ovarian aging to cardiovascular risk. The absence of consistent associations across analyses suggests that alternative pathways may underlie this relationship. Further research incorporating a broader range of biomarkers is warranted to elucidate the complex interactions between reproductive aging and cardiovascular health in women.</p>","PeriodicalId":16610,"journal":{"name":"Journal of Ovarian Research","volume":"18 1","pages":"164"},"PeriodicalIF":4.2,"publicationDate":"2025-07-26","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC12297770/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144717975","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":"hnRNPA2B1 restrains granulosa cell ferroptosis by m⁶A/SLC7A11 in premature ovarian failure.","authors":"Jing Xiong, Ling He, Yongjing Zhang, Xing Zhao","doi":"10.1186/s13048-025-01718-y","DOIUrl":"10.1186/s13048-025-01718-y","url":null,"abstract":"<p><p>Premature ovarian failure (POF) is a relatively severe gynecological disorder that is often accompanied by other systemic diseases. Here, this study identified that N⁶-methyladenosine (m⁶A) key enzyme heterogeneous nuclear ribonucleoprotein A2/B1 (hnRNPA2B1) was associated with POF pathophysiological process. In the chemotherapy induced POF animal and cells, hnRNPA2B1 was down-regulated upon cisplatin (CDDP) treatment. Functionally, hnRNPA2B1 inhibited the ferroptosis phenotype by m⁶A/SLC7A11 of granulosa cells. Moreover, hnRNPA2B1 up-regulated the autophagy by inhibiting PI3K/AKT/mTOR pathway of granulosa cells. Besides, rescue experiments confirmed that hnRNPA2B1/SLC7A11 axis repressed the ferroptosis of granulosa cells through m⁶A-dependent manner. In summary, the research identified the critical role of hnRNPA2B1 in granulosa cells ferroptosis, which provides novel insight for POF treatment.</p>","PeriodicalId":16610,"journal":{"name":"Journal of Ovarian Research","volume":"18 1","pages":"165"},"PeriodicalIF":4.2,"publicationDate":"2025-07-26","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC12297619/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144717974","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}