• 文献检索
  • 文档翻译
  • 深度研究
  • 学术资讯
  • Suppr Zotero 插件Zotero 插件
  • 邀请有礼
  • 套餐&价格
  • 历史记录
应用&插件
Suppr Zotero 插件Zotero 插件浏览器插件Mac 客户端Windows 客户端微信小程序
定价
高级版会员购买积分包购买API积分包
服务
文献检索文档翻译深度研究API 文档MCP 服务
关于我们
关于 Suppr公司介绍联系我们用户协议隐私条款
关注我们

Suppr 超能文献

核心技术专利:CN118964589B侵权必究
粤ICP备2023148730 号-1Suppr @ 2026

文献检索

告别复杂PubMed语法,用中文像聊天一样搜索,搜遍4000万医学文献。AI智能推荐,让科研检索更轻松。

立即免费搜索

文件翻译

保留排版,准确专业,支持PDF/Word/PPT等文件格式,支持 12+语言互译。

免费翻译文档

深度研究

AI帮你快速写综述,25分钟生成高质量综述,智能提取关键信息,辅助科研写作。

立即免费体验

多囊卵巢综合征界面附近GnRH神经元-神经胶质细胞网络的改变:分子机制与临床前景

Altered GnRH neuron-glia networks close to interface of polycystic ovary syndrome: Molecular mechanism and clinical perspectives.

作者信息

Dai Ruoxi, Sun Yan

机构信息

Hospital & Institute of Obstetrics and Gynecology, Fudan University, Shanghai 200081, China.

Hospital & Institute of Obstetrics and Gynecology, Fudan University, Shanghai 200081, China; The Academy of Integrative Medicine, Fudan University, Shanghai 200081, China; Shanghai Key Laboratory of Female Reproductive Endocrine-related Disease, Shanghai 200081, China.

出版信息

Life Sci. 2025 Jan 15;361:123318. doi: 10.1016/j.lfs.2024.123318. Epub 2024 Dec 22.

DOI:10.1016/j.lfs.2024.123318
PMID:39719166
Abstract

Polycystic ovary syndrome (PCOS) has been noticed as a neuroendocrine syndrome manifested by reproductive hormone dysregulation involving increased luteinizing hormone (LH) pulse frequency and an increased LH to follicle-stimulating hormone ratio, yet theory is just beginning to be established. Neuroglia located in the arcuate nucleus and median eminence (ARC-ME) that are close to gonadotropin-releasing hormone (GnRH) axon terminals, comprise the blood-brain barrier and fenestrated vessels implying their putative roles in the modulation of the abnormal GnRH pulse in PCOS. This review outlines the disturbances of neuron-glia networks that underlie hypothetically the deregulation of GnRH-LH release and impaired sex hormone negative feedback in PCOS. We then discuss chronic and low-grade inflammatory status together with gut dysbiosis and how the detriments may intrude the hypothalamus by virtue of violating interfaces between the brain and periphery, which might contribute to the etiology of the impaired neural circuits in the ARC-ME to induce PCOS.

摘要

多囊卵巢综合征(PCOS)已被视为一种神经内分泌综合征,其表现为生殖激素失调,包括促黄体生成素(LH)脉冲频率增加以及LH与促卵泡激素的比值升高,但其理论才刚刚开始建立。位于弓状核和正中隆起(ARC-ME)的神经胶质细胞靠近促性腺激素释放激素(GnRH)轴突终末,构成血脑屏障和有窗孔的血管,这意味着它们在调节PCOS中异常GnRH脉冲方面可能发挥作用。本综述概述了神经元-神经胶质细胞网络的紊乱,这些紊乱假设是PCOS中GnRH-LH释放失调和性激素负反馈受损的基础。然后,我们讨论了慢性低度炎症状态以及肠道菌群失调,以及这些损害如何通过破坏大脑与外周之间的界面侵入下丘脑,这可能导致ARC-ME中神经回路受损的病因,从而诱发PCOS。

相似文献

1
Altered GnRH neuron-glia networks close to interface of polycystic ovary syndrome: Molecular mechanism and clinical perspectives.多囊卵巢综合征界面附近GnRH神经元-神经胶质细胞网络的改变:分子机制与临床前景
Life Sci. 2025 Jan 15;361:123318. doi: 10.1016/j.lfs.2024.123318. Epub 2024 Dec 22.
2
Activation of arcuate nucleus GABA neurons promotes luteinizing hormone secretion and reproductive dysfunction: Implications for polycystic ovary syndrome.弓状核 GABA 神经元的激活可促进黄体生成素的分泌和生殖功能障碍:对多囊卵巢综合征的影响。
EBioMedicine. 2019 Jun;44:582-596. doi: 10.1016/j.ebiom.2019.05.065. Epub 2019 Jun 6.
3
Enhancement of a robust arcuate GABAergic input to gonadotropin-releasing hormone neurons in a model of polycystic ovarian syndrome.在多囊卵巢综合征模型中增强对促性腺激素释放激素神经元的强大弓形γ-氨基丁酸能输入。
Proc Natl Acad Sci U S A. 2015 Jan 13;112(2):596-601. doi: 10.1073/pnas.1415038112. Epub 2014 Dec 30.
4
GnRH pulse generator activity in mouse models of polycystic ovary syndrome.多囊卵巢综合征小鼠模型中的促性腺激素释放激素脉冲发生器活性
Elife. 2025 Jan 6;13:RP97179. doi: 10.7554/eLife.97179.
5
Sex and Time of Day Alter the Interactions Between Hypothalamic Glia and the Neural Circuits Controlling Reproduction.性别和一天中的时间会改变下丘脑神经胶质细胞与控制生殖的神经回路之间的相互作用。
Endocrinology. 2025 Mar 24;166(5). doi: 10.1210/endocr/bqaf057.
6
Effects of electroacupuncture on the kisspeptin-gonadotropin-releasing hormone (GnRH) /luteinizing hormone (LH) neural circuit abnormalities and androgen receptor expression of kisspeptin/neurokinin B/dynorphin neurons in PCOS rats.电针对多囊卵巢综合征大鼠 kisspeptin-促性腺激素释放激素(GnRH)/黄体生成素(LH)神经回路异常及 kisspeptin/神经激肽 B/强啡肽神经元雄激素受体表达的影响。
J Ovarian Res. 2023 Jan 17;16(1):15. doi: 10.1186/s13048-022-01078-x.
7
Increase of kisspeptin-positive cells in the hypothalamus of a rat model of polycystic ovary syndrome.多囊卵巢综合征大鼠模型下丘脑弓状核中 kisspeptin 阳性细胞数量增加。
Metab Brain Dis. 2016 Jun;31(3):673-81. doi: 10.1007/s11011-016-9807-0. Epub 2016 Feb 11.
8
Activation of a Classic Hunger Circuit Slows Luteinizing Hormone Pulsatility.激活经典饥饿回路可减缓黄体生成素脉冲性分泌。
Neuroendocrinology. 2020;110(7-8):671-687. doi: 10.1159/000504225. Epub 2019 Oct 21.
9
Chronic androgen excess in female mice does not impact luteinizing hormone pulse frequency or putative GABAergic inputs to GnRH neurons.慢性雄性激素过多症在雌性小鼠中并不影响黄体生成素脉冲频率或 GnRH 神经元的 GABA 能传入。
J Neuroendocrinol. 2022 Apr;34(4):e13110. doi: 10.1111/jne.13110. Epub 2022 Mar 10.
10
Pathological pulses in PCOS.多囊卵巢综合征的病理性脉象。
Mol Cell Endocrinol. 2019 Dec 1;498:110561. doi: 10.1016/j.mce.2019.110561. Epub 2019 Aug 25.

引用本文的文献

1
Decoding androgen excess in polycystic ovary syndrome: Roles of insulin resistance and other key intraovarian and systemic factors.解读多囊卵巢综合征中的雄激素过多:胰岛素抵抗及其他关键的卵巢内和全身因素的作用
World J Diabetes. 2025 Jul 15;16(7):108789. doi: 10.4239/wjd.v16.i7.108789.
2
Regulatory risk loci link disrupted androgen response to pathophysiology of Polycystic Ovary Syndrome.调控风险位点将雄激素反应紊乱与多囊卵巢综合征的病理生理学联系起来。
medRxiv. 2025 Mar 27:2025.03.26.25324630. doi: 10.1101/2025.03.26.25324630.