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线粒体稳态调控卵巢生理学的机制。

Mechanism of Mitochondrial Homeostasis Controlling Ovarian Physiology.

机构信息

Clinical Medical College, Key Laboratory of Fertility Preservation and Maintenance of Ministry of Education, School of Basic Medical Sciences, Ningxia Medical University, Yinchuan 750004, China.

出版信息

Endocrinology. 2022 Nov 14;164(1). doi: 10.1210/endocr/bqac189.

DOI:10.1210/endocr/bqac189
PMID:36378567
Abstract

Ovarian cells, including oocytes, granulosa/cumulus cells, theca cells, and stromal cells, contain abundant mitochondria, which play indispensable roles in the processes of ovarian follicle development. Ovarian function is closely controlled by mitochondrial proteostasis and mitostasis. While mitochondrial proteostasis and mitostasis are disturbed by several factors, leading to dysfunction of ovarian function and initiating the mitochondrial unfolded protein response (UPRmt) and mitophagy to maintain or recover ovarian function and mitochondrial function, clear interactions between the 2 pathways in the ovary have not been fully elucidated. Here, we comprehensively summarize the molecular networks or regulatory mechanisms behind further mitochondrial research in the ovary. This review provides novel insights into the interactions between the UPRmt and mitophagy in ovarian functions.

摘要

卵巢细胞,包括卵母细胞、颗粒细胞/卵泡细胞、膜细胞和基质细胞,含有丰富的线粒体,这些线粒体在卵泡发育过程中起着不可或缺的作用。卵巢功能受线粒体蛋白质稳态和线粒体稳定的密切控制。尽管线粒体蛋白质稳态和线粒体稳定受到多种因素的干扰,导致卵巢功能障碍并启动线粒体未折叠蛋白反应(UPRmt)和线粒体自噬来维持或恢复卵巢功能和线粒体功能,但这两条途径在卵巢中的相互作用尚未完全阐明。在这里,我们全面总结了卵巢进一步线粒体研究背后的分子网络或调节机制。本综述为 UPRmt 和线粒体自噬在卵巢功能中的相互作用提供了新的见解。

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