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REVIEW ARTICLE
Year : 2021  |  Volume : 11  |  Issue : 3  |  Page : 207-215

Nutrigenetic reprogramming of oxidative stress


1 Department of Ophthalmology, Jonas Children's Vision Care and the Bernard and Shirlee Brown Glaucoma Laboratory, Columbia Stem Cell Initiative, Columbia University, New York, NY, USA
2 Department of Ophthalmology, Jonas Children's Vision Care and the Bernard and Shirlee Brown Glaucoma Laboratory, Columbia Stem Cell Initiative; Department of Ophthalmology, Institute of Human Nutrition, Columbia University, New York, NY; Department of Ophthalmology, The University of Texas Rio Grande Valley School of Medicine, Edinburg, TX, USA
3 Department of Ophthalmology, Jonas Children's Vision Care and the Bernard and Shirlee Brown Glaucoma Laboratory, Columbia Stem Cell Initiative, Columbia University, New York, NY; Department of Ophthalmology, State University of New York at Downstate Medical Center, Brooklyn, USA
4 Department of Ophthalmology, Jonas Children's Vision Care and the Bernard and Shirlee Brown Glaucoma Laboratory, Columbia Stem Cell Initiative; Department of Ophthalmology, Institute of Human Nutrition, Columbia University, New York, NY, USA
5 Department of Ophthalmology, Jonas Children's Vision Care and the Bernard and Shirlee Brown Glaucoma Laboratory, Columbia Stem Cell Initiative; Department of Ophthalmology, Columbia University, New York, USA
6 Department of Ophthalmology, Jonas Children's Vision Care and the Bernard and Shirlee Brown Glaucoma Laboratory, Columbia Stem Cell Initiative; Department of Ophthalmology, Institute of Human Nutrition; Department of Pathology and Cell Biology, College of Physicians and Surgeons, Institute of Human Nutrition, Columbia University, NY, USA

Correspondence Address:
Dr. Stephen H Tsang
Edward Harkness Eye Institute, 635 W 165th Street, Box 212, New York, NY 10032
USA
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Source of Support: None, Conflict of Interest: None


DOI: 10.4103/tjo.tjo_4_21

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Retinal disorders such as retinitis pigmentosa, age-related retinal degeneration, oxygen-induced retinopathy, and ischemia-reperfusion injury cause debilitating and irreversible vision loss. While the exact mechanisms underlying these conditions remain unclear, there has been a growing body of evidence demonstrating the pathological contributions of oxidative stress across different cell types within the eye. Nuclear factor erythroid-2-related factor (Nrf2), a transcriptional activator of antioxidative genes, and its regulator Kelch-like ECH-associated protein 1 (Keap1) have emerged as promising therapeutic targets. The purpose of this review is to understand the protective role of the Nrf2-Keap1 pathway in different retinal tissues and shed light on the complex mechanisms underlying these processes. In the photoreceptors, we highlight that Nrf2 preserves their survival and function by maintaining oxidation homeostasis. In the retinal pigment epithelium, Nrf2 similarly plays a critical role in oxidative stabilization but also maintains mitochondrial motility and autophagy-related lipid metabolic processes. In endothelial cells, Nrf2 seems to promote proper vascularization and revascularization through concurrent activation of antioxidative and angiogenic factors as well as inhibition of inflammatory cytokines. Finally, Nrf2 protects retinal ganglion cells against apoptotic cell death. Importantly, we show that Nrf2-mediated protection of the various retinal tissues corresponds to a preservation of functional vision. Altogether, this review underscores the potential of the Nrf2-Keap1 pathway as a powerful tool against retinal degeneration. Key insights into this elegant oxidative defense mechanism may ultimately pave the path toward a universal therapy for various inherited and environmental retinal disorders.


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