The Relationship Between Ferroptosis and Premature Ovarian Insufficiency

doi:10.12280/gjfckx.20240412

Abstract

Abstract:

Premature ovarian insufficiency (POI) is a complex condition that not only leads to perimenopausal symptoms, but also affects female fertility and overall physical and mental health. Once ovarian function is impaired, it is irreversible. Therefore, exploring the pathogenic mechanisms of POI and delaying its progression are paramountly important. Recent studies have revealed a close relationship between ferroptosis and POI. Ferroptosis is an iron-dependent form of cell death that regulates a variety of cellular biological processes in the body. Oxidative stress, autophagy, abnormal iron metabolism, and lipid metabolism disorders can induce ferroptosis, damaging ovarian function. Additionally, abnormal activation of the Hippo/Yes-associated protein (YAP) and tumor protein p53 (TP53) / nuclear factor erythroid 2-related factor 2 (Nrf2) signaling pathway can also impair ovarian function though ferroptosis. Moreover, research has found that activation of glutathione peroxidase 4 (GPX4), ferrostatin-1 (Fer-1), and Coenzyme Q10 (CoQ10) can effectively reduce ferroptosis, suggesting these as potential therapeutic targets for future treatment of POI.

Key words: Ferroptosis, Primary ovarian insufficiency, Ovarian follicle, Signal transduction, Oxidative stress, Premature ovarian insufficiency

GAO Yi-wei, LUO Wei, WU Qiong, MU Yu-lan. The Relationship Between Ferroptosis and Premature Ovarian Insufficiency[J]. Journal of International Obstetrics and Gynecology, 2024, 51(5): 497-502.

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