Researchers in Australia have identified genes that play a role in oxidative stress and aging in the macula.
A team of researchers from CERA, the University of Melbourne, Lions Eye Institute and other Australian collaborators, led by CERA’s Principal Investigator of Cellular Reprogramming Associate Professor Raymond Wong, have for the first time found that the genes TMEM97 and POLDIP2 play a role in regulating oxidative stress – a part of ageing in the macula.
The findings, published in Aging1 and the International Journal of Molecular Science2, provide a deeper understanding of the underlying causes of AMD and help prioritize new gene targets for treatments.
Previous studies have identified many genes that are linked to AMD, though Associate Professor Wong’s team are the first to investigate the roles of two specific genes, TMEM97 and POLDIP2, in human retinal pigmented epithelial cells (RPE) – the cells affected in AMD.
To determine the genes’ function, the team created a model of human RPE cells in the lab. Then, researchers switched off the two genes, discovering they had a key role in maintaining cell health.
“It turns out both of these genes play roles in regulating the oxidative stresses, which is a key mechanism in ageing of the retina,” Associate Professor Wong says. “Generally high oxidative stress is bad for cells – and could contribute to RPE degeneration.”
These findings have opened the door for further research into the genetic causes of AMD, as well as the potential for developing future AMD treatments targeting the genes regulating cell degeneration.