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Pathogenesis of keratoconus: NRF2-antioxidant, extracellular matrix and cellular dysfunctions.

Authors
  • Monteiro de Barros, Maithê Rocha1
  • Chakravarti, Shukti2
  • 1 Department of Ophthalmology, NYU Grossman School of Medicine, NY, 10016, USA. Electronic address: [email protected]
  • 2 Department of Ophthalmology, NYU Grossman School of Medicine, NY, 10016, USA; Department of Pathology, NYU Grossman School of Medicine, NY, 10016, USA. Electronic address: [email protected]
Type
Published Article
Journal
Experimental Eye Research
Publisher
Elsevier
Publication Date
Apr 03, 2022
Volume
219
Pages
109062–109062
Identifiers
DOI: 10.1016/j.exer.2022.109062
PMID: 35385756
Source
Medline
Keywords
Language
English
License
Unknown

Abstract

Keratoconus (KC) is a degenerative disease associated with cell and extracellular matrix (ECM) loss that causes gradual thinning and steepening of the cornea and loss of vision. Collagen cross linking with ultraviolet light treatment can strengthen the ECM and delay weakening of the cornea, but severe cases require corneal transplantation. KC is multifactorial and multigenic, but its pathophysiology is still an enigma. Multiple approaches are being pursued to elucidate the molecular changes that underlie the corneal phenotype to identify relevant genes for tailored candidate searches and to develop potential biomarkers and targets for therapeutic interventions. Recent proteomic and transcriptomic studies suggest dysregulations in oxidative stress, NRF2-regulated antioxidant programs, WNT-signaling, TGF-β, ECM and matrix metalloproteinases. This review aims to provide a broad update on the transcriptomic and proteomic studies of KC with a focus on findings that relate to oxidative stress, and dysregulations in cellular and extracellular matrix functions. Copyright © 2022. Published by Elsevier Ltd.

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