A new study published in Aging Cell and co-authored by Doheny scientists, Drs. Sreekumar Parameswaran, Ram Kannan, and Srinivas Sadda shed new light on why some people with neovascular age-related macular degeneration (nAMD) develop permanent vision loss. nAMD, often called “wet AMD,” is an advanced form of macular degeneration in which abnormal blood vessels grow under the retina. These fragile vessels leak fluid and blood, damaging the cells responsible for sharp, central vision. Treatment for patients with wet AMD includes ocular injections of therapies that stop the growth of abnormal vessels. Over time, some patients experience a complication called subretinal fibrosis, a type of retinal scarring that can cause irreversible vision loss.

The study looks at a protein called OGC, which helps important eye cells called retinal pigment epithelial (RPE) cells keep their “energy centers,” or mitochondria, working well. When these cells lose energy, they can change into cells that create scar tissue, a process called epithelial-to-mesenchymal transition (EMT). Researchers discovered that when there is insufficient OGC, the harmful change to EMT happens faster, and the cells make more scar tissue. But when there is more OGC, the cells stay healthier, and the scarring slows down. Mouse models confirmed the pattern: animals with less OGC developed much more scarring in their eyes. Until now, the link between mitochondrial health and this scarring response had not been well understood.

Why It Matters

These findings identify OGC as a promising new therapeutic target for preventing the scarring that leads to vision loss in wet AMD. While treatments based on this pathway are still on the horizon, studies like this underscore the vital importance of continued investment in vision research. Each discovery brings us closer to new therapies that can preserve sight and protect millions from blinding diseases.