首页|内质网应激在多囊卵巢综合征中的研究进展

内质网应激在多囊卵巢综合征中的研究进展

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多囊卵巢综合征(polycystic ovary syndrome,PCOS)是一种常见的妇科内分泌疾病,患者通常伴有月经失调、不孕、多毛、痤疮和肥胖等临床表现,目前确切的发病机制尚不清楚。近年越来越多的证据显示内质网应激(endoplasmic reticulum stress)参与了PCOS的病理过程,有望成为治疗PCOS的新靶点。内质网应激是内质网的稳态失衡,未折叠或错误折叠的蛋白质在内质网中积累的状态。一定程度的内质网应激有助于卵泡的发育成熟,但持续的内质网应激会诱导颗粒细胞凋亡,并且通过影响类固醇激素代谢、糖代谢和脂质代谢等过程导致PCOS患者卵泡发育异常、性激素及胰岛素合成分泌紊乱,从而对女性生育能力造成不利影响。综述内质网应激与PCOS各种致病因素之间的关系,以期为PCOS的病因学研究和治疗提供新思路。
Advances of Endoplasmic Reticulum Stress in Polycystic Ovary Syndrome
Polycystic ovary syndrome(PCOS)is a prevalent gynecological endocrine disorder characterized by menstrual disorders,infertility,hirsutism,acne and obesity.The precise pathogenesis of PCOS remains unclear.Recent evidence has demonstrated the involvement of endoplasmic reticulum stress in its pathological process,suggesting the potential of endoplasmic reticulum stress as a novel therapeutic target for PCOS.Endoplasmic reticulum stress refers to the state where the endoplasmic reticulum is in a state of steady imbalance and the accumulation of incorrectly folded or unfolded proteins in the endoplasmic reticulum.Moderate endoplasmic reticulum stress contributes to the development and maturation of follicles.Sustained endoplasmic reticulum stress leads to the abnormal follicle development,hormonal and insulin synthesis and secretion disorders in PCOS patients by inducing granulosa cell apoptosis and mediating processes such as steroid hormone metabolism,glucose metabolism and lipid metabolism,thereby impairing female fertility.This paper provides an overview of the relationship between endoplasmic reticulum stress and various pathogenic factors associated with PCOS,to offer fresh insights into its etiology and treatment.

Polycystic ovary syndromeEndoplasmic reticulum stressFollicular developmentHyperandrogenismInsulin resistanceObesity

李文雅、张巧利、杨晓葵

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100026 首都医科大学附属北京妇产医院/北京妇幼保健院生殖医学科

多囊卵巢综合征 内质网应激 卵泡发育 雄激素增多症 胰岛素抵抗 肥胖症

北京市医院管理中心"登峰"人才培养计划

DFL20191401

2024

国际生殖健康/计划生育杂志
天津市医学科学技术信息研究所

国际生殖健康/计划生育杂志

CSTPCD
影响因子:0.694
ISSN:1674-1889
年,卷(期):2024.43(1)
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