Abstract
Presentation Description :
The presentation will outline how endogenous and exogenous oxidative stress combined with genetic factors and cellular post-mitotic arrest leads to endothelial cell loss in Fuchs endothelial corneal dystrophy.In addition it will show that chronic accumulation of oxidative DNA damage contributes to the corneal endothelial cell degeneration by causing loss of mitochondrial membrane potential, mitochondrial fragmentation and apoptosis in FECD. Therefore, therapies targetting aging and oxidative stress pathways could provide alternatives to corneal transpantation for FECD patients. Morover, lifestyle and environmental modifications could be applied to Fuchs patients, similarly to what is being done for other age-related ocular disorders.
This is an abstract that was submitted for the 2018 ARVO Annual Meeting, held in Honolulu, Hawaii, April 29 - May 3, 2018.