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

IF 5.2 2区医学 Q1 MEDICINE, RESEARCH & EXPERIMENTAL

Life sciences Pub Date : 2025-01-15 DOI:10.1016/j.lfs.2024.123318

Ruoxi Dai , Yan Sun

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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.

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多囊卵巢综合征界面附近GnRH神经元-胶质细胞网络的改变：分子机制和临床观点。

多囊卵巢综合征（PCOS）被认为是一种以生殖激素失调为表现的神经内分泌综合征，包括促黄体生成素（LH）脉冲频率增加和促卵泡生成素与促卵泡生成素之比增加，但理论才刚开始建立。位于弓形核和正中隆起（ARC-ME）的神经胶质细胞靠近促性腺激素释放激素（GnRH）轴突末端，构成血脑屏障和开孔血管，这意味着它们在PCOS中GnRH异常脉冲的调节中可能起作用。这篇综述概述了神经元-胶质细胞网络的紊乱，这些紊乱可能是多囊卵巢综合征中GnRH-LH释放失调和性激素负反馈受损的基础。然后，我们讨论了慢性和低度炎症状态以及肠道生态失调，以及这些损害如何通过破坏大脑和外周之间的界面侵入下丘脑，这可能有助于ARC-ME神经回路受损的病因，从而诱发多囊卵巢综合征。

本文章由计算机程序翻译，如有差异，请以英文原文为准。

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来源期刊

Life sciences 医学-药学

CiteScore

12.20

自引率

1.60%

发文量

841

审稿时长

6 months

期刊介绍： Life Sciences is an international journal publishing articles that emphasize the molecular, cellular, and functional basis of therapy. The journal emphasizes the understanding of mechanism that is relevant to all aspects of human disease and translation to patients. All articles are rigorously reviewed. The Journal favors publication of full-length papers where modern scientific technologies are used to explain molecular, cellular and physiological mechanisms. Articles that merely report observations are rarely accepted. Recommendations from the Declaration of Helsinki or NIH guidelines for care and use of laboratory animals must be adhered to. Articles should be written at a level accessible to readers who are non-specialists in the topic of the article themselves, but who are interested in the research. The Journal welcomes reviews on topics of wide interest to investigators in the life sciences. We particularly encourage submission of brief, focused reviews containing high-quality artwork and require the use of mechanistic summary diagrams.