Mitochondrial dysfunction and oxidative stress in corneal disease

Neeru A. Vallabh, Vito Romano, Colin Willoughby

    Research output: Contribution to journal › Article

    12 Citations (Scopus)

    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.
    LanguageEnglish
    Pages103-113
    JournalMitochondrion
    Volume36
    Early online date23 May 2017
    DOIs
    Publication statusE-pub ahead of print - 23 May 2017

    Fingerprint

    Corneal Diseases
    Cornea
    Oxidative Stress
    Mitochondrial DNA
    Kearns-Sayre Syndrome
    Fuchs' Endothelial Dystrophy
    Corneal Endothelium
    Keratoconus
    Mitochondrial Genome
    DNA Damage
    Reactive Oxygen Species
    Endothelial Cells
    Antioxidants
    Radiation
    Oxygen
    Mutation

    Keywords

    • Antioxidants
    • Cornea
    • Fuchs endothelial dystrophy
    • Kearns Sayre Syndrome
    • Keratoconus
    • Mitochondria
    • Oxidative stress

    Cite this

    Vallabh, Neeru A. ; Romano, Vito ; Willoughby, Colin. / Mitochondrial dysfunction and oxidative stress in corneal disease. In: Mitochondrion. 2017 ; Vol. 36. pp. 103-113.
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    Vallabh, NA, Romano, V & Willoughby, C 2017, 'Mitochondrial dysfunction and oxidative stress in corneal disease', Mitochondrion, vol. 36, pp. 103-113. https://doi.org/10.1016/j.mito.2017.05.009

    Mitochondrial dysfunction and oxidative stress in corneal disease. / Vallabh, Neeru A.; Romano, Vito; Willoughby, Colin.

    In: Mitochondrion, Vol. 36, 23.05.2017, p. 103-113.

    Research output: Contribution to journal › Article

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    AU - Willoughby, Colin

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    N2 - 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.

    AB - 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.

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    Vallabh NA, Romano V, Willoughby C. Mitochondrial dysfunction and oxidative stress in corneal disease. Mitochondrion. 2017 May 23;36:103-113. https://doi.org/10.1016/j.mito.2017.05.009

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