Diabetic retinopathy is one of a number of nasty effects diabetes can have on the human body. The disease sees the development of leaky blood vessels in the eye that over time lead to permanent loss of vision. Though it is the leading cause of new cases of blindness in American adults, its progress can be slowed by certain drugs or laser treatment. But research has now uncovered a new protein found to drive the condition, raising the possibility of preventing it altogether.
Said to affect between 40 and 45 percent of American diabetics, diabetic retinopathy takes hold as the eye's regular blood vessels are taken over by abnormal, fragile vessels that leak into the eye. These unwelcome fluids then cause damage to the retina that can be difficult to notice in the early stages, but if left untreated, can eventually lead to permanent damage or blindness.
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There are a number of ways diabetic retinopathy can be treated, though none of them are perfect. In the beginning, better control of blood sugar can slow its progress. More advanced diabetic retinopathy can require laser treatments to seal the vessels and stop the leakage, but this can compromise peripheral and night-time vision. Several drugs have also been developed that can neutralize VEGF, a growth factor that gives rise to the dangerous and leaky blood vessels, but these have been found to be unreliable in preventing the condition on their own.
It is the hope of researchers at the John Hopkins University that this little glimmer of hope offered by VEGF-blocking drugs could be combined with something more to offer a complete solution. The scientists took samples of eye fluid from healthy people, diabetics with diabetic retinopathy and also diabetics without it. The team found that though VEGF levels were generally higher in those with diabetic retinopathy, in some subjects the fluid was less VEGF-heavy even than the healthy participants, suggesting something else was at play.
A number of experiments followed using human cells and mice, and the team came to identify VEGF's partner in crime, a protein called angiopoietin-like 4. It found that by blocking activity of the new protein and VEGF at the same time, it was able to greatly slow the abnormal blood vessel growth in lab-grown cells.
The researchers are now exploring whether the newly-identified culprit angiopoietin-like 4 is a factor in macular degeneration and other diseases that slowly but surely cause damage to the retina. They say that if a drug can be found that effectively inhibits activity of angiopoietin-like 4, it could be partnered with VEGF-blocking drugs to prevent the onset of diabetic retinopathy.
The research findings will be published online in the journal Proceedings of the National Academy of Sciences on May 25.
Source: John Hopkins University