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. 2021 Mar 5;12:649295. doi: 10.3389/fphys.2021.649295

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Copyright © 2021 Xu and Wang.

This is an open-access article distributed under the terms of the Creative Commons Attribution License (CC BY). The use, distribution or reproduction in other forums is permitted, provided the original author(s) and the copyright owner(s) are credited and that the original publication in this journal is cited, in accordance with accepted academic practice. No use, distribution or reproduction is permitted which does not comply with these terms.

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Regulation and contribution of FoxO1 activity in the pathogenesis of polycystic ovary syndrome (PCOS). FoxO1 activity is mainly regulated by the post-translational modifications, including phosphorylation, acetylation, and ubiquitination. FoxO1 is involved in the pathogenesis of PCOS through various signaling pathways, including phosphoinositide 3-kinase (PI-3K)/protein kinase B (PKB), mitogen-activated protein kinase (MAPK), high-mobility group box 1(HMGB1)/Toll-like receptor 4(TLR4)/nuclear factor-kappa B (NF-κB), and Interleukin-1β (IL-1β).