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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.

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。

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