C Verhaeghe, K J Lindquist, M E Bleil, M Rosen, R F Redberg, D Haisenleder, C E McCulloch, Marcelle I Cedars
{"title":"卵巢老化、心血管风险和炎症:来自OVA研究的见解。","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":null,"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":4.2000,"publicationDate":"2025-07-26","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC12297770/pdf/","citationCount":"0","resultStr":"{\"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\":null,\"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\":4.2000,\"publicationDate\":\"2025-07-26\",\"publicationTypes\":\"Journal Article\",\"fieldsOfStudy\":null,\"isOpenAccess\":false,\"openAccessPdf\":\"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC12297770/pdf/\",\"citationCount\":\"0\",\"resultStr\":null,\"platform\":\"Semanticscholar\",\"paperid\":null,\"PeriodicalName\":\"Journal of Ovarian Research\",\"FirstCategoryId\":\"3\",\"ListUrlMain\":\"https://doi.org/10.1186/s13048-025-01754-8\",\"RegionNum\":3,\"RegionCategory\":\"医学\",\"ArticlePicture\":[],\"TitleCN\":null,\"AbstractTextCN\":null,\"PMCID\":null,\"EPubDate\":\"\",\"PubModel\":\"\",\"JCR\":\"Q1\",\"JCRName\":\"REPRODUCTIVE BIOLOGY\",\"Score\":null,\"Total\":0}","platform":"Semanticscholar","paperid":null,"PeriodicalName":"Journal of Ovarian Research","FirstCategoryId":"3","ListUrlMain":"https://doi.org/10.1186/s13048-025-01754-8","RegionNum":3,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":null,"EPubDate":"","PubModel":"","JCR":"Q1","JCRName":"REPRODUCTIVE BIOLOGY","Score":null,"Total":0}
Ovarian aging, cardiovascular risk and inflammation: insights from the OVA study.
Background: 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.
Results: 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.
Conclusion: 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.
期刊介绍:
Journal of Ovarian Research is an open access, peer reviewed, online journal that aims to provide a forum for high-quality basic and clinical research on ovarian function, abnormalities, and cancer. The journal focuses on research that provides new insights into ovarian functions as well as prevention and treatment of diseases afflicting the organ.
Topical areas include, but are not restricted to:
Ovary development, hormone secretion and regulation
Follicle growth and ovulation
Infertility and Polycystic ovarian syndrome
Regulation of pituitary and other biological functions by ovarian hormones
Ovarian cancer, its prevention, diagnosis and treatment
Drug development and screening
Role of stem cells in ovary development and function.