September 2016
Volume 57, Issue 12
Open Access
ARVO Annual Meeting Abstract  |   September 2016
Mitophagy in Fuchs Endothelial Corneal Dystrophy
Author Affiliations & Notes
  • Ula V Jurkunas
    MA Eye & Ear Infirm Schepens Eye Res, Boston, Massachusetts, United States
  • Footnotes
    Commercial Relationships   Ula Jurkunas, 61/482,769 (P), ClearView Healthcare (C), Dana and Wiggin (C), Santen (C)
  • Footnotes
    Support  R01 EY020581
Investigative Ophthalmology & Visual Science September 2016, Vol.57, No Pagination Specified. doi:
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    • Get Citation

      Ula V Jurkunas; Mitophagy in Fuchs Endothelial Corneal Dystrophy. Invest. Ophthalmol. Vis. Sci. 201657(12):.

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      © ARVO (1962-2015); The Authors (2016-present)

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Presentation Description : Corneal endothelium is a cell layer specifically susceptible to aging due to its post-mitotic arrest, high metabolic activity due to pumping of ions, and lifelong exposure to ultraviolet (UV) light. Because endothelium has minimal replicative capacity in vivo and inability to replace its genome, it is specifically prone to cumulative DNA damage acquired throughout the lifetime of an individual. In Fuchs endothelial corneal dystrophy (FECD), the underlying genetic defects render the genome of corneal endothelial cells even more susceptible to this damage, to the point of causing dysfunction of the power houses of the cells, mitochondria. Our studies detected an increase in mitochondrial and nuclear DNA damage in FECD which led to the loss of mitochondrial membrane potential, decrease in ATP levels, and subsequent mitochondrial fission. Upregulation of mitophagy was noted to account for enhanced fission and loss of mitochondrial mass in FECD. The presentation will outline the dysfunction of specific mitophagy pathways involved the development of FECD.

This is an abstract that was submitted for the 2016 ARVO Annual Meeting, held in Seattle, Wash., May 1-5, 2016.


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