Researchers at the University of Michigan Kellogg Eye Center have identified a compound that could interrupt the chain of events that cause damage to the retina in diabetic retinopathy. The finding is significant because it could lead to a novel therapy that targets two mechanisms at the root of the disease: inflammation and the weakening of the blood barrier that protects the retina.
To date, treatments for diabetic retinopathy, the leading cause of blindness among working-age Americans, have been aimed largely at one of those mechanisms.
In diabetic retinopathy, damage to the retina results, in part, from the activity of vascular endothelial growth factor (VEGF), a protein that weakens the protective blood-retinal barrier. Recent drugs targeting VEGF have exhibited good response for nearly half of the patients with diabetic retinopathy. But researchers believe that there is also an inflammatory component that may contribute to the disease process.
The study, published in the Biochemical Journal, June 2012 [epub ahead of print] identifies a specific protein common to both pathways as an important target in regulating the disease process in which blood vessels become leaky, and provides a drug that may be developed into a therapeutic intervention for patients in which anti-VEGF treatment alone is not sufficient.