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Review
. 2022 Aug 10;23(16):8927.
doi: 10.3390/ijms23168927.

Epigenetic Regulation of Optic Nerve Development, Protection, and Repair

Ajay Ashok  1 , Sarita Pooranawattanakul  1 , Wai Lydia Tai  1 , Kin-Sang Cho  1 , Tor P Utheim  2   3 , Dean M Cestari  1 , Dong Feng Chen  1
Affiliations
Review

Epigenetic Regulation of Optic Nerve Development, Protection, and Repair

Ajay Ashok et al. Int J Mol Sci. .

Abstract

Epigenetic factors are known to influence tissue development, functionality, and their response to pathophysiology. This review will focus on different types of epigenetic regulators and their associated molecular apparatus that affect the optic nerve. A comprehensive understanding of epigenetic regulation in optic nerve development and homeostasis will help us unravel novel molecular pathways and pave the way to design blueprints for effective therapeutics to address optic nerve protection, repair, and regeneration.

Keywords: epigenetics; myelin; oligodendrocytes; optic nerve; regeneration.

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Conflict of interest statement

The authors declare no conflict of interest.

Figures

Figure 1
Figure 1
Epigenetic regulation of gene expression. Enhanced translational activity occurs after chromatin structure attains an open configuration, generally following DNA and histone demethylation and histone acetylation. This dynamic epigenetic mechanism is fueled by a group of enzymes that are categorized by their characteristic of presenting or reverting the methyl and acetyl groups on the histone or DNA structure. DNMT: DNA methyltransferase; TET: Ten-eleven translocation enzymes; HDAC: histone deacetylase; HAT: histone acetylase; HMT: histone methyl transferase; HDM: histone demethylase; Me: methyl group; Ac: acetyl group.
Figure 2
Figure 2
HDAC inhibitors rescue RGCs by modulating the histone acetylation levels. HDAC families I, II, and III are known to upregulate significantly in glaucoma models [64]. Blocking HDAC activity using inhibitors offers significant neuroprotection, including enhanced RGC protection. HDAC activity inhibition reprograms the chromatin structure to a pro-translational configuration which occurs through modulation of factors such as p53, CREB-binding protein/p300 (CBP/p300), and the p300-CBP-associated factor (P/CAF), which facilitate neuroprotection, etc. [67,68]. Ac: acetyl group.
See this image and copyright information in PMC

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