Epigenetics and Regulation of Oxidative Stress in Diabetic Retinopathy
Author(s) -
Arul J. Duraisamy,
Manish Mishra,
Anjaneyulu Kowluru,
Renu A. Kowluru
Publication year - 2018
Publication title -
investigative ophthalmology and visual science
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.935
H-Index - 218
eISSN - 1552-5783
pISSN - 0146-0404
DOI - 10.1167/iovs.18-24548
Subject(s) - nadph oxidase , oxidative stress , rac1 , small interfering rna , biology , reactive oxygen species , chemistry , microbiology and biotechnology , endocrinology , biochemistry , transfection , signal transduction , gene
Oxidative stress plays a central role in the development of diabetic retinopathy, and in the pathogenesis of this blinding disease, activation of NADPH oxidase 2 (Nox2)-mediated cytosolic reactive oxygen species (ROS) production precedes mitochondrial damage. The multicomponent cytosolic Nox2 has an obligatory component, Ras-related C3 botulinum toxin substrate 1 (Rac1); in diabetes, Rac1 is functionally and transcriptionally active. Diabetes also facilitates many epigenetic modifications, and activates both DNA methylating (Dnmts) and hydroxymethylating (Tets) enzymes. Our aim was to investigate the role of epigenetics in Rac1 regulation in diabetes.
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