Scientists are looking at ways of creating new therapies that will help to prevent the development of eye disease in people with diabetes.
Researchers from the Schepens Eye Research Institute in Massachusetts in the United States have found that a slight increase in transforming growth factor beta (TGF-ß), which is present in preclinical animal models with diabetic eye disease, protects against diabetic retinopathy.
The condition occurs when retinal blood vessels are damaged and leak fluid. It is the most common cause of eye problems for people with diabetes including blindness.
‘We found that increased TGF-ß is really defending the vessels in the retina,’ said senior author Mara Lorenzi, recently retired senior scientist at Schepens Eye Research Institute of Massachusetts and Eye and Ear and Professor of Ophthalmology at Harvard Medical School.
‘When we took away the small increase in TGF-ß, we saw significant damage to the retinal vessels in animals with diabetes. Based on this finding, we’d now like to know if a little extra TGF-ß will help protect the retinal vessels in patients with diabetes,’ she explained.
In light of these findings, the study authors also caution the use of anti-TGF-ß therapies, which have been studied to prevent damage from diabetes in other parts of the body, such as the kidneys.
She explained that an accumulation of fluid into the retina can lead to swelling at the centre of the retina (macular edema). As diabetes related damage progresses, the vessels become blocked and can no longer carry blood. New blood vessels grow on the surface of the retina but can leak or rupture, impairing vision.
The study authors had previously found an increased level of TGF-ß in diabetic retinal blood vessels so for this study they set out to investigate whether increased TGF-ß was responsible for the development of diabetic retinopathy. They used a medication to block the increased, but not baseline, TGF-ß signalling in a diabetic rat model.
The authors were surprised to find that taking away the small increase in TGF-ß resulted in damage to the retinal vessels in the diabetic rat. This led them to conclude that TGF-ß protects the retinal vessels, and that inhibiting its effects will likely accelerate retinopathy in diabetic patients.
Based on this finding, the study authors not only caution the use of TGF-ß blocking as a therapy for diabetes, but also suggest that there may be ways to identify drugs for upward modulation of TGF-ß signalling in a very controlled fashion to prevent or delay diabetic retinopathy.
Currently, there are no treatments for diabetic retinopathy beyond controlling blood glucose and blood pressure levels. The new vessels can be treated with laser techniques, but this is at the expense of damage to the retina.
‘There is definitely room for intervening early to protect the retina from diabetes. Our hope is that a good TGF-ß response to diabetes may protect patients from developing diabetic retinopathy, and that our findings may inspire new approaches toward this objective,’ added Lorenzi.
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