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程序性细胞死亡因子 4:多囊卵巢综合征发病机制中的一个新角色。

Programmed cell death 4: A novel player in the pathogenesis of polycystic ovary syndrome.

机构信息

Women's Reproductive Health Research Center, Tabriz University of Medical Sciences, Tabriz, Iran.

Department of Biochemistry and Clinical Laboratories, Faculty of Medicine, Tabriz University of Medical Sciences, Tabriz, Iran.

出版信息

Cell Biochem Funct. 2024 Jan;42(1):e3905. doi: 10.1002/cbf.3905. Epub 2023 Dec 19.

DOI:10.1002/cbf.3905
PMID:38115175
Abstract

Polycystic ovary syndrome (PCOS) is a pathological condition recognized by menstrual cycle irregularities, androgen excess, and polycystic ovarian morphology, affecting a significant proportion of women of childbearing age and accounting for the most prevalent cause of anovulatory sterility. In addition, PCOS is frequently accompanied by metabolic and endocrine disturbances such as obesity, dyslipidemia, insulin resistance, and hyperinsulinemia, indicating the multiplicity of mechanisms implicated in the progression of PCOS. However, the exact pathogenesis of PCOS is yet to be elucidated. Programmed cell death 4 (PDCD4) is a ubiquitously expressed protein that contributes to the regulation of various cellular processes, including gene expression, cell cycle progression, proliferation, and apoptosis. Despite some disparities concerning its exact cellular effects, PDCD4 is generally characterized as a protein that inhibits cell cycle progression and proliferation and instead drives the cell into apoptosis. The apoptosis of granulosa cells (GCs) is speculated to take a major part in the occurrence and progression of PCOS by ceasing antral follicle development and compromising oocyte competence. Given the possible involvement of GC apoptosis in the progression of PCOS, as well as the contribution of PDCD4 to the regulation of cell apoptosis and the development of metabolic diseases, the current review aimed to discuss whether or how PDCD4 can play a role in the pathogenesis of PCOS by affecting GC apoptosis.

摘要

多囊卵巢综合征(PCOS)是一种以月经周期不规律、雄激素过多和多囊卵巢形态为特征的病理状态,影响了相当一部分育龄妇女,是无排卵性不孕的最常见原因。此外,PCOS 常伴有代谢和内分泌紊乱,如肥胖、血脂异常、胰岛素抵抗和高胰岛素血症,表明 PCOS 进展涉及多种机制。然而,PCOS 的确切发病机制仍未阐明。程序性细胞死亡因子 4(PDCD4)是一种广泛表达的蛋白质,参与调节多种细胞过程,包括基因表达、细胞周期进程、增殖和细胞凋亡。尽管 PDCD4 的确切细胞作用存在一些差异,但 PDCD4 通常被认为是一种抑制细胞周期进程和增殖、促使细胞凋亡的蛋白质。颗粒细胞(GCs)的凋亡被认为通过停止窦卵泡发育和损害卵母细胞的能力,在 PCOS 的发生和进展中起主要作用。鉴于 GC 凋亡可能参与 PCOS 的进展,以及 PDCD4 对细胞凋亡调节和代谢性疾病发展的贡献,本综述旨在讨论 PDCD4 是否以及如何通过影响 GC 凋亡来发挥作用在 PCOS 的发病机制中。

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