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. 2022 Jan 5;12:788535. doi: 10.3389/fendo.2021.788535

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Copyright © 2022 Wang, Ma, Wang, Sun, Wang, Li, Liu and Yu

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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Potential mechanism of epigenetics and gut microbiome in the pathogenesis of GO. Abnormal epigenetic modifications may promote pro-inflammatory cascades and disrupt the expression of signaling molecules that are involved in the fibrogenesis and adipogenesis of orbital fibroblasts. Gut microbiome possibly drives the pathogenesis of GO by influencing secretion of TRAb and Th17/Treg imbalance. The process of all these changes will lead to the hyaluronan production and the activation of orbital fibroblasts, which eventually develop into tissue expansion, fibrosis and inflammation. LMG, lowly methylated genes; HMG, highly methylated genes; TRAb, Thyrotropin receptor antibody; Treg, regulatory T; Th17, T-helper 17.