Infectious Keratitis: An Update on Role of Epigenetics

Abstract

Epigenetic mechanisms modulate gene expression and function without altering the base sequence of DNA. These reversible, heritable, and environment-influenced mechanisms generate various cell types during development and orchestrate the cellular responses to external stimuli by regulating the expression of genome. Also, the epigenetic modifications influence common pathological and physiological responses including inflammation, ischemia, neoplasia, aging and neurodegeneration etc. In recent past, the field of epigenetics has gained momentum and become an increasingly important area of biomedical research As far as eye is concerned, epigenetic mechanisms may play an important role in many complex diseases such as corneal dystrophy, cataract, glaucoma, diabetic retinopathy, ocular neoplasia, uveitis, and age-related macular degeneration. Focusing on the epigenetic mechanisms in ocular diseases may provide new understanding and insights into the pathogenesis of complex eye diseases and thus can aid in the development of novel treatments for these diseases. In the present review, we summarize the clinical perspective of infectious keratitis, role of epigenetics in infectious keratitis, therapeutic potential of epigenetic modifiers and the future perspective.

Keywords: epigenetics; histone modifications; infectious; keratitis; methylation.

Figure 1

Key epigenetic modifications in common ocular diseases: Diverse epigenetic modifications are associated with the common ocular diseases occurring in different parts of the eye. MMP2, matrix metalloproteinase 2; CD24, CD24 molecule; TGM2, transglutaminase 2; hsa-miR, human microRNA; GSTP1, pi-class glutathione-S-transferase; OGG1, 8-oxoguanine DNA glycosylase 1; ERCC6, excision repair 6 chromatin remodeling factor; CRYAA, crystalline Alpha-A; TGFBIp, transforming growth factor β- induced; GSTM1/5, glutathione S-transferase isoform mu1/mu5; IL17RC, interleukin-17 receptor C; MSH6, mutS homolog 6; CD44, cluster of differentiation 44; PAX5, paired box 5; GATA5, GATA binding protein 5; TP53, tumor protein 53; VHL, Von Hippel-Lindau gene; GSTP1, glutathione S-transferase pi-1; MGMT, methylguanine methyltransferase; RB1, retinoblastoma 1; CDKN2, cyclin-dependent kinase inhibitor 2; 5hmC, 5-hydroxymethyl cytosine; RAC1, rac family small GTPase 1; LOXL1, lysyl oxidase-like 1; TGF-β1, transforming growth factor-β1; RASSF1A, RAS association domain family 1A gene; TM, trabecular meshwork; LC, the lamina cribrosa.

Figure 2

Infectious keratitis caused by different agents: (A) Bacterial keratitis (B) Fungal keratitis (C) Herpes necrotizing stromal keratitis (D) Early Acanthamoeba keratitis (E) Late Acanthamoeba keratitis. Adopted from https://www.intechopen.com/chapters/69696 under Creative Commons Attribution 3.0 License.