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. 2024 Aug 20;15:1450440. doi: 10.3389/fimmu.2024.1450440

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Copyright © 2024 Wang, Feng, Ni, Wang, Zhang, Cao, Zhou and Zhao

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 of histone modifications in diabetic wound healing, by mediating macrophage-mediated inflammation. The modification site and modification type are shown on H3 and H4. MOF can acetylate lysine 16 on the histone H4 (H4K16) and regulate NF-κB-mediated inflammatory cytokine expression, thus leading to inflammation and delayed diabetic wound healing. MLL1 can methylate lysine 4 on histone H3 (H3K4) and regulate the COX-2/PGE2 pathway, promoting the expression of inflammatory cytokines, thus leading to inflammation and delayed diabetic wound healing. Setdb2 can methylate lysine 9 on histone 3 (H3K9) and regulate NF-κB-mediated inflammatory cytokine expression and production of uric acid, thus leading to inflammation and delayed diabetic wound healing. JMJD3 can demethylate the lysine 27 site on histone 3 (H3K27) to regulate NF-κB-mediated inflammatory cytokine expression, modulating inflammation and causing delayed diabetic wound healing. This figure was created with the aid of Biorender (https://biorender.com/).