New Delhi: US scientists have found the answer to why treatment for neonatal age-related macular degeneration (AMD) – a leading cause of blindness – does not benefit everyone; and also developed a potential antibody treatment. AMD is a condition characterized by abnormal blood vessel growth in the back of the eye. Aging, diabetes, obesity and many other chronic metabolic diseases cause excessive vascular growth and There is damage to the VEGF – the part of the eye that converts light into image signals. The first line of defense is usually anti-VEGF therapy, which blocks vascular endothelial growth factor and prevents excessive blood vessel growth. However, the team at the Medical College of Georgia (MCG) said this only works well for about a third of patients. They found that the cause is “fibroblast cells.” The collagen and several other proteins produced by these fibroblast cells “Accumulate outside the vascular cells and eventually cause fibrosis or scarring in the eye. This is prevented by suppression of excess vasculature by anti-VEGF treatments,” the study published.
“In this study, for the first time, we show that many fibroblast cells are actually produced by these highly endothelial cells,” said Yuqing Huo, director of the Vascular Inflammation Program at MCG’s Vascular Biology Center, in the journal Science Translational Medicine. For, the team targeted adenosine receptor 2A (Adora2A) – a G-protein-coupled adenosine receptor found at high levels in the brain, immune cells, and blood vessels. Although inflammation, myocardial oxygen consumption and coronary blood flow Adenosine is important in controlling inflammation, but in high doses, adenosine can cause excessive blood vessel growth. Using genetically engineered mice that developed fibrosis in the back of their eyes, researchers used an Adora2A agonist. (KW6002), which binds to the receptor and blocks its function. The team said the mice showed a reduction in fibrosis in the eyes. “An antibody can actually prevent both excessive blood vessel growth, the early stage of AMD, and fibrosis, the late stage of AMD. Our findings indicate that blocking Adora2a “This could certainly target multiple stages of the disease, which could be far more efficient than current treatments,” Huo said.
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2024-05-03 02:35:42