Researchers led by scientists at UCL have discovered a protein that appears to set off diabetic retinopathy, a common eye disease caused by high blood sugar damaging the retina’s blood vessels. The condition is one of the leading causes of vision loss among working-age adults. The study, published in Science Translational Medicine, points to a protein called LRG1 as a key factor that triggers the earliest stage of retinal damage after diabetes develops.
The researchers found that LRG1 causes cells surrounding the eye’s tiniest blood vessels to tighten excessively and squeeze them. This constriction reduces oxygen delivery to the retina and begins a chain reaction that can eventually lead to long-term vision impairment. In experiments using diabetic mouse models, scientists were able to block the activity of LRG1. When they did so, the early retinal damage did not occur and normal eye function was preserved.
Advantages Over Existing Treatments
Diabetic retinopathy affects people with both type 1 and type 2 diabetes. In many cases, treatment only begins once symptoms such as blurred or distorted vision appear. By that point, significant and irreversible damage may have already occurred. Existing treatments focus on another protein called VEGF. However, these therapies work for only about half of patients and typically do not reverse the harm that has already developed.
The new research suggests that LRG1 begins driving eye damage much earlier than VEGF. Because of this, scientists believe it may represent a promising new target for therapy. A treatment designed to block LRG1 could potentially intervene earlier and stop the disease from progressing. The UCL research team has already created a drug designed to target LRG1. The treatment has been tested in earlier studies and is currently undergoing additional preclinical research. Scientists say it could move into human clinical trials in the near future.
This article is an AI-assisted summary. All facts and figures are drawn from the original report: https://www.sciencedaily.com/releases/2026/03/260306224225.htm