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. 2022 Mar 29;9:868788. doi: 10.3389/fcvm.2022.868788

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Copyright © 2022 Yang, Sun, Li, Jin and Dai.

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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Different lysine methyltransferases may play opposite roles of in macrophage polarization and functions. (A) H3K4me3 mediated by lysine methyltransferases (KMTs e.g., KMT2A/MLL) is involved in oxLDL-induced training immunity of monocytes (Mo) in atherosclerosis (AS) and LPS-induced M1 polarization. (B) High-fat diet (HFD) induces the expression of TRPA1 (a calcium permeable non-selective cation channel), which stabilizes EZH2 (PRC2 or KMT6) to inhibit M1 polarization via H3K27me3. (C) LPS and IFNs up-regulates SETDB2 via IRF7, while deletion of SETDB2 in hematopoietic cells promotes M1-like polarization and impairs efferocytosis, a function of M2 macrophages, via H3K9me3 in AS lesions. oxLDL, oxidized low-density lipoprotein; LPS, lipopolysaccharide; TRPA1, transient receptor potential ankyrin 1; EZH2, enhancer of zeste homolog 2; IFN, interferon; IRF7, interferon regulatory factor 7; SETDB2, SET domain bifurcated histone lysine methyltransferase 2.