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. 2021 Nov 23;12:784591. doi: 10.3389/fphar.2021.784591

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Copyright © 2021 Cai, Gan, Tang, Wu and Gao.

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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Underlying mechanisms of histone modifications in CLDs. The main histone modifications, the targeted genes, the corresponding effects and the therapeutic targets in CLDs were shown. (A) Modifications of histones are mediated via writers and erasers, and are recognized by readers. These modifications work through changing the expression of corresponding genes. (B) In ALD, p300, HDAC, and BRD4 mediate the histone modifications at specific genes, which regulate lipid and alcohol metabolisms and inflammation reaction. (C) In MAFLD, p300/CBP, HDAC1, SET7/9 et al. mediate the histone modifications at specific genes, which promote chronic inflammation, lipid and glucose metabolism and oxidative stress. (D) In viral hepatitis, PRMT5, HDAC1, BRD4 et al. mediate the histone modifications at specific genes, which regulate HBV replication, cccDNA accumulation and transcription. (E) In autoimmune liver disease, p300 and other proteins mediate the histone modifications at specific genes, which promote T cell proliferation, INF production and cholangiocyte senescence. (F) In liver fibrosis/cirrhosis, p300, SET7/9, HDAC 3 et al. mediate the histone modifications at specific genes, which promote HSC activation, ECM accumulation and chronic inflammation. ALD: alcoholic liver disease; MAFLD: metabolic-associated fatty liver disease; HSC: hepatic stellate cell; IFN: interferon; ECM: extracellular matrix.