Iron, as an essential trace element for the organism, is vital for maintaining the organism's health. Excessive iron can promote reactive oxygen species (ROS) accumulation, thus damaging cells and tissues. Ferroptosis is a novel form of programmed cell death distinguished by iron overload and lipid peroxidation, which is unique from autophagy, apoptosis and necrosis, more and more studies are focusing on ferroptosis. Recent evidence suggests that ferroptosis is associated with the development of female reproductive disorders (FRDs), including polycystic ovary syndrome (PCOS), premature ovarian insufficiency (POI), endometriosis (EMs), ovarian cancer (OC), preeclampsia (PE) and spontaneous abortion (SA). Pathways and genes associated with ferroptosis may participate in processes that regulate granulosa cell proliferation and secretion, oocyte development, ovarian reserve function, early embryonic development and placental oxidative stress. However, its exact mechanism has not been fully revealed. Therefore, our review systematically elaborates the occurrence mechanism of ferroptosis and its research progress in the development of FRDs, with a view to providing literature references for clinical targeting of ferroptosis -related pathways and regulatory factors for the management of FRDs.
Keywords: Female reproductive disorders; Ferroptosis; Iron metabolism; Lipid metabolism; Reactive oxygen species; System Xc(-)-GSH-GPX4 pathway.
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