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. 2022 Sep 20;10:60. doi: 10.1038/s41413-022-00226-9

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© The Author(s) 2022

Open Access This article is licensed under a Creative Commons Attribution 4.0 International License, which permits use, sharing, adaptation, distribution and reproduction in any medium or format, as long as you give appropriate credit to the original author(s) and the source, provide a link to the Creative Commons license, and indicate if changes were made. The images or other third party material in this article are included in the article’s Creative Commons license, unless indicated otherwise in a credit line to the material. If material is not included in the article’s Creative Commons license and your intended use is not permitted by statutory regulation or exceeds the permitted use, you will need to obtain permission directly from the copyright holder. To view a copy of this license, visit http://creativecommons.org/licenses/by/4.0/.

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Fig. 1 — Epigenetic regulation of osteoarthritis. Three types of epigenetic regulation of the molecular pathogenesis of OA. a DNA methylation is catalyzed by DNMTs, and abnormal changes in DNA methylation occur in the promoter regions of related genes and signaling pathways in OA chondrocytes. b Histone modifications included phosphorylation, methylation, acetylation, ubiquitination, and SUMOylation. Histone acetylation is mainly mediated by HATs, and histone deacetylation is usually catalyzed by two types of enzymes: classic histone deacetylases (HDACs) and sirtuins. Increased H3K4 methylation leads to catabolic responses mediated by iNOS and COX-2 expression in human OA chondrocytes. The methylation of H3K9 increases Sox9 and mPGES-1 expression in human OA chondrocytes. c MiR-204/miR-211, miR-181a-5p, miR-335-5p, and miR-93 inhibit Runx2, chondrocyte apoptosis, and the expression of catabolic and hypertrophic genes