Mitochondrial dysfunction and oxidative stress in corneal disease

Vallabh, Neeru A ORCID: 0000-0002-0109-4112, Romano, Vito ORCID: 0000-0002-5148-7643 and Willoughby, Colin E (2017) Mitochondrial dysfunction and oxidative stress in corneal disease. MITOCHONDRION, 36. pp. 103-113.

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Abstract

The cornea is the anterior transparent surface and the main refracting structure of the eye. Mitochondrial dysfunction and oxidative stress are implicated in the pathogenesis of inherited (e.g. Kearns Sayre Syndrome) and acquired corneal diseases (e.g. keratoconus and Fuchs endothelial corneal dystrophy). Both antioxidants and reactive oxygen species are found in the healthy cornea. There is increasing evidence of imbalance in the oxidative balance and mitochondrial function in the cornea in disease states. The cornea is vulnerable to mitochondrial dysfunction and oxidative stress due to its highly exposed position to ultraviolet radiation and high oxygen tension. The corneal endothelium is vulnerable to accumulating mitochondrial DNA (mtDNA) damage due to the post- mitotic nature of endothelial cells, yet their mitochondrial genome is continually replicating and mtDNA mutations can develop and accumulate with age. The unique physiology of the cornea predisposes this structure to oxidative damage, and there is interplay between inherited and acquired mitochondrial dysfunction, oxidative damage and a number of corneal diseases. By targeting mitochondrial dysfunction in corneal disease, emerging treatments may prevent or reduce visual loss.

Item Type:	Article
Uncontrolled Keywords:	Cornea, Mitochondria, Antioxidants, Oxidative stress, Keratoconus, Fuchs endothelial dystrophy, Kearns Sayre Syndrome
Depositing User:	Symplectic Admin
Date Deposited:	01 Jun 2017 09:07
Last Modified:	19 Jan 2023 07:03
DOI:	10.1016/j.mito.2017.05.009
Related URLs:	Author Publisher
URI:	https://livrepository.liverpool.ac.uk/id/eprint/3007768