New approach for Treating and Preventing Diabetic Retinopathy

by Dr. Trupti Shirole on May 27 2015 9:20 AM

New approach for Treating and Preventing Diabetic Retinopathy
Diabetic retinopathy is the most common diabetic eye disease that can lead to blindness. It occurs when normal blood vessels of the eye are replaced over time with abnormal, fragile blood vessels that leak fluid or bleed into the eye, damaging the light-sensitive retina and causing blindness. About 40-45% of Americans with diabetes have diabetic retinopathy, according to the US National Eye Institute. US researchers have now found a new way to restore the eyesight in patients with diabetic retinopathy by blocking a second blood vessel growth protein, along with one that is already well-known. This can help in treating and preventing diabetic retinopathy.
Researchers at the Johns Hopkins University and the University of Maryland said, "Laser-sealing eye blood vessels can save central vision, but this often sacrifices peripheral and night vision." Several recently developed drugs, bevacizumab, ranibizumab and aflibercept, can help treat these blood vessels by blocking the action of VEGF, a so-called growth factor released as part of a chain of signals in response to low oxygen levels, which stimulates the growth of new, often abnormal, blood vessels. Lead author Akrit Sodhi, an assistant professor of ophthalmology at the Johns Hopkins University School of Medicine said, "But studies have shown that although these drugs slow progression to proliferative diabetic retinopathy, it does not reliably prevent it."

To find an explanation, researchers tested levels of VEGF in samples of fluid from the eye taken from healthy people, people with diabetes who did not have diabetic retinopathy and people with diabetic retinopathy of varying severity. While levels of VEGF tended to be higher in people with proliferative diabetic retinopathy, some of their fluid had less VEGF than did the healthy participants. But even the low-VEGF fluid from those with proliferative diabetic retinopathy stimulated blood vessel growth in lab-grown cells. Sodhi said, "The results suggested to us that although VEFG clearly plays an important role in blood vessel growth, it’s not the only factor."

A series of experiments in laboratory-grown human cells and mice revealed a second culprit, a protein called angiopoietin-like 4. When the researchers blocked the action of both VEGF and angiopoietin-like 4 in fluid from the eyes of patients with proliferative diabetic retinopathy, it markedly reduced blood vessel growth in lab-grown cells. Sodhi said, "If a drug can be found that safely blocks the second protein’s action in patients’ eyes, it might be combined with the anti-VEGF drugs to prevent many cases of proliferative diabetic retinopathy."

The research team is now investigating whether angiopoietin-like 4 might also play a role in other eye diseases, such as macular degeneration, which destroys the central portion of the retina.