Researchers from UVA Health have found a new factor that makes eye blood vessels grow in a harmful way. This exciting discovery could be the start of new treatments for macular degeneration and other problems that can make your vision worse.
Jayakrishna Ambati and Shao-bin Wang from the University of Virginia (UVA) have identified something that could possibly stop strange blood vessels entangling in the eye, which is seen with conditions like neovascular age-related macular degeneration, proliferative diabetic retinopathy, and ischemic retinal vein occlusion.
Dr. Ambati from the University of Virginia School of Medicine’s Department of Ophthalmology believes that we can fight eye diseases by targeting a certain part in our body. This part is called “epigenetic machinery”.
We did some research on how the immune cells in eyes cause loss of control over blood vessels and now have a better understanding. This will help us to create better, cheaper, and more accessible treatments to avoid things like drug resistance, which is becoming an increasing problem with existing treatments.
New Discoveries in Treating Age-Related Macular Degeneration with FTO Protein
Scientists have noticed that a substance called VEGF is causing too much blood vessel growth in the eye. So, doctors have treatments for it which can help but the benefits usually don’t last long. This means that doctors need to find better treatments to make sure people don’t lose their eyesight.
Ambati and Wang’s new study has discovered a special protein that affects the VEGF quantity in lab mice. When this protein was blocked from the mice, their VEGF levels dropped considerably without causing any harm to their eyes such as the area which can cause vessel overgrowth.
Scientists discovered that FTO, a type of protein previously linked to obesity in humans, is also connected to how our eyes develop. It affects ocular neovascularization, which means it helps control the growth of new blood vessels under the retina. This was an answer scientists had been looking for over 20 years!
Scientists from the UVA just made a discovery that could help millions of people around the world who suffer from vision loss. This finding can explain why blood vessels grow too much and damage someone’s sight. Over 200 million people in the world have this condition, called neurovascular age-related macular degeneration. While more research and tests are necessary before a treatment becomes available, scientists think this breakthrough has great potential to really make a difference!
“We don’t have the best way to treat eye diseases that involve extra blood vessels growing. So, it’s important for us to find other cures. Our research can help create new treatments and make dealing with these kinds of illnesses easier,” said Wang.
A recent study published in the journal Signal Transduction and Targeted Therapy has found that targeting a particular type of enzyme called m6A mRNA demethylase FTO can help suppress the release of vessel growth factor and choroidal neovascularization. This research was conducted by Shao-bin Wang, Yosuke Nagasaka, Dionne Argyle, Ayami Nagasaka, Praveen Yerramothu, Bradley D. Gelfand and Jayakrishna Ambati on February 20th, 2023.
Ambati is the founder of several companies such as DiceRx, iVeena Holdings, iVeena Delivery Systems, and Inflammasome Therapeutics. He has also did work that was not related to research. All of the authors’ necessary information can be found in the paper.
Several different people and organizations helped finance this study including; The National Institutes of Health, The UVA Strategic Investment Fund, The DuPont Guerry III professorship, gifts from Mr. and Mrs. Eli W Tullis, Annette Lightner Fund, BrightFocus Foundation Award and Owens Family Foundation.
Journal Reference: Shao-bin Wang, Yosuke Nagasaka, Dionne Argyle, Ayami Nagasaka, Praveen Yerramothu, Bradley D. Gelfand, Jayakrishna Ambati. Targeting the m6A mRNA demethylase FTO suppresses vascular endothelial growth factor release and choroidal neovascularization. Signal Transduction and Targeted Therapy, 2023; 8 (1) DOI: 10.1038/s41392-022-01277-4
