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. 2022 Mar 10;16:823708. doi: 10.3389/fncel.2022.823708

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Copyright © 2022 Li, Xiao and Chen.

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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A working model of histone acetylation and methylation underlying OLs dysfunction in schizophrenia. Histone acetylation and methylation at the promoters governing the expression of oligodendrocyte/myelin-related (OMR) genes. Multiple sites of H3 and H4 are dynamically regulated by histone acetyltransferases/deacetylases (e.g., HATs, HDACs) and/or histone methyltransferases/demethylases (e.g., KMTs, KDMs, and PRMTs). The cross-talk between two classes of enzymes secures the balance of epigenetic marks in OLs. In schizophrenia, the dysregulation of enzymes could change the balance/priority of histone acetylation and methylation at some key sites (e.g., H3K9), thus induce the reactivation of OL differentiation inhibitors and increase the cellular susceptibility. ac, histone acetylation; me, histone methylation; H3, histone 3; H4, histone 4.