Oxidative damage to the mitochondrial DNA of corneal cells may be the cause of Fuchs’ Endothelial Corneal Dystrophy (FECD), a common age-related eye disease that affects around 4 percent of the population.

Researchers at Schepens Eye Research Institute of Massachusetts Eye and Ear found that in FECD, the mitochondria of the corneal endothelium die and break up due to lifelong accumulated oxidative damage caused by UV light and cell processes.

Because corneal endothelial cells do not divide in humans, dead cells are not replaced, leading to corneal swelling and blindness if left untreated, and the only current treatment option is a corneal transplant.

The next step, according the researchers, is to develop therapies which protect corneal endothelial cells from damage. Ula Jurkunas, lead investigator on the study, said, “This is a significant advancement in that process and moves us one step closer to our ultimate goal, which is to provide FECD patients with alternative and safer treatments options to transplantation.”

Further information: http://www.masseyeandear.org/news/press-releases/2016/03/new-research-links-mitochondrial-dysfunction-to-development-of-fuchs-endothelial-corneal-dystrophy