Protein may block diabetic retinopathy damage


Researchers have identified a protein, atypical protein kinase C (aPKC), that may help regulate the process that causes damage in diabetic retinopathy.

Ann Arbor, MI-A protein that could “interrupt” the chain of events that causes retinal damage in diabetic retinopathy has been identified by researchers at the University of Michigan Kellogg Eye Center. The finding could lead to a therapy that targets two mechanisms at the root of the disease: inflammation and the weakening of the blood barrier that protects the retina.

Drugs targeting vascular endothelial growth factor (VEGF) have exhibited good response for many patients with diabetic retinopathy, but researchers believe that an inflammatory component also may contribute to the disease process.

In a study published in the Biochemical Journal, the researchers said that a specific protein, atypical protein kinase C (aPKC), is common to both pathways as an important target in regulating the disease process. The discovery may lead to the development of a therapeutic intervention for patients in whom anti-VEGF treatment alone is not sufficient.

In addition to regulating the disease process, the researchers said aPKC also is effective at blocking damage from tumor necrosis factor, which also is elevated in diabetic retinopathy and contributes to part of the inflammation.

“This is a great leap forward,” said David A. Antonetti, PhD, professor, department of ophthalmology and visual sciences and molecular and integrative physiology, Kellogg Eye Center, University of Michigan.

“We’ve identified an important target in regulating blood vessel leakage in the eye and we have a therapy that works in animal models,” Dr. Antonetti said. “Our research is in the early stages of development. We still have a long way to go to demonstrate effectiveness of this compound in humans to create a new therapy, but the results are very promising.”

For more articles in this issue of Ophthalmology Times eReport, click here.

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