Mitochondrial dysfunction and oxidative stress in corneal disease

Neeru A. Vallabh, Vito Romano, Colin Willoughby

    Research output: Contribution to journalArticlepeer-review

    71 Citations (Scopus)


    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.
    Original languageEnglish
    Pages (from-to)103-113
    Early online date23 May 2017
    Publication statusPublished online - 23 May 2017


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


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