UCL Researchers Identify LRG1 Protein as Primary Trigger for Early Stage Diabetic Blindness in Global Breakthrough

UCL scientists identify LRG1 as the protein causing early diabetic eye damage. Blocking this protein could prevent blindness before symptoms begin.

By: AXL Media

Published: Mar 7, 2026, 6:21 AM EST

Source: The information in this article was sourced from UCL

A New Biological Target for Retinal Protection

A research team led by University College London (UCL) has identified a protein called LRG1 as the key driver behind the initial stages of diabetic retinopathy. According to the study published in Science Translational Medicine on March 4, 2026, this protein is responsible for the very first signs of damage in the eye following the onset of diabetes. By pinpointing this specific biological trigger, researchers believe they have found a way to intervene in the disease's progression far earlier than currently possible, potentially sparing millions of patients from the leading cause of blindness in working-age adults.

The Mechanism of Early Retinal Squeezing

The study reveals a previously unknown mechanical process where LRG1 causes cells surrounding the retina's smallest blood vessels to contract excessively. According to lead author Dr. Giulia De Rossi, this contraction "squeezes" the vessels, severely restricting oxygen delivery to the light-sensing cells of the eye. This localized oxygen deprivation sets off a destructive chain reaction that eventually leads to the distorted vision and permanent blindness associated with advanced diabetes. In laboratory experiments, blocking LRG1 in diabetic mice completely prevented this vascular constriction, preserving normal ocular function despite high blood sugar levels.

Limitations of Current Anti VEGF Therapies

Existing treatments for diabetic eye disease primarily focus on a different protein known as VEGF, which is involved in the later stages of the condition when new, leaky blood vessels begin to grow. However, clinical data shows that these treatments only work for approximately half of all patients and rarely reverse the damage that has already occurred. According to co-author Professor John Greenwood, the discovery of LRG1 is "enormously exciting" because it acts as an initiating factor that predates the involvement of VEGF. This suggests that targeting LRG1 could offer a solution for the significant percentage of patients who do not respond to traditional therapies.