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Scientists search for new treatment target for diabetic retinopathy

by Medical Xpress
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Scientists at the Medical College of Georgia at Augusta University are searching for a new treatment target for a common complication of diabetes that can cause retinal blood vessels to break down, leak, or become blocked.

Diabetic retinopathy is a serious eye disease and a leading cause of blindness that results when diabetes’ sustained high blood sugar levels cause damage to the retina—the part of the eye that detects light—over time. That can happen in a number of ways, from inflammation to overgrowth of new and abnormal blood vessels.

The current treatment standard is anti-VEGF, which targets and blocks the activity of vascular endothelial growth factor (VEGF), a protein that promotes the growth of blood vessels and causes them to leak. But that treatment doesn’t work for everyone.

Vascular and endothelial biologist Shruti Sharma, Ph.D., and a team from the MCG Center for Biotechnology and Genomic Medicine, hope to zero in on a new treatment pathway. They suspect the key to that may be a protein called Interleukin-6 (IL-6), a versatile protein involved in both immunity and inflammation throughout the body.

“IL-6 is a major cytokine that is elevated in almost all inflammatory conditions,” Sharma explained. “There have been therapies that have targeted IL-6, but whenever we try to completely block it, that never seems to work. I don’t think it’s that black or white.”

She and her research team think the answer lies in the way IL-6 signals or initiates physiological changes in the body. One mechanism involves cis-signaling, where IL-6 interacts with its receptor on the cell surface, while the other involves trans-signaling, which uses a soluble form of IL-6 receptor.

The harmful inflammatory effects of IL-6 are accomplished mainly through trans-signaling, while beneficial regenerative effects are accomplished through cis-signaling.

“So that’s where the problem was. When you’re globally blocking all the IL-6, you are taking away the good and the bad,” Sharma said.

“We already know that trans-signaling works through endothelial cells, because they lack the membrane-bound receptor, which would explain the inflammation and overgrowth of blood vessels in the eye.”

In preliminary studies, she and her research team found that blocking the pro-inflammatory IL-6 trans-signaling, with a drug called sgp130Fc, helped balance levels of two important proteins in the retina—VEGFA, which can damage the blood-retina barrier and increase , and VEGFB, which is believed to be protective. They believe that disruption to that balance is what ultimately leads to the development of .

They hope finding the way to restore that balance will come from taking a closer look at Müller glial cells, which play a major role in maintaining homeostasis and exchange of nutrients in the retina. They also have membrane-bound IL-6 receptors and “participate” in both cis- and trans-signaling. “There are also certain factors released by these that help activate ,” Sharma said.

They will study several different animal models—one that uses trans-signaling, one that uses cis-signaling and one that does both—and gather baseline measurements of the photoreceptor response, which can tell them how well the eye can detect light, a key indicator of retinal health or disease.

“We believe that when we selectively inhibit trans-signaling using this drug, while allowing cis-signaling to continue, we will be able to stop the damage,” Sharma said.

A recent global analysis estimated that about 103 million people worldwide have diabetic retinopathy, and that number could rise to 161 million by 2045.

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Scientists search for new treatment target for diabetic retinopathy (2024, September 12)
retrieved 12 September 2024
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