Diabetes affects hundreds of millions of people worldwide, and one of its most feared complications is vision loss. High blood sugar over long periods can damage small blood vessels throughout the body, including those in the eyes.
This damage can lead to a condition called diabetic retinopathy, which is one of the leading causes of blindness among working-age adults.
For many people, the disease develops slowly and without clear warning signs until vision has already been seriously affected. Because of this, doctors and scientists have long searched for ways to detect and stop the disease before permanent damage occurs.
Now a team of researchers led by scientists at University College London (UCL) has discovered a protein that appears to play a crucial role in starting the disease process. Their findings suggest that diabetic eye disease may begin earlier than previously believed and may be driven by a specific molecular signal.
The research was published in the journal Science Translational Medicine and was supported by organizations including Diabetes UK, Moorfields Eye Charity, and the Wellcome Trust.
The researchers identified a protein called LRG1 as a key factor that triggers the earliest stages of damage in the retina. The retina is a thin layer of tissue at the back of the eye that detects light and sends visual signals to the brain. It contains a dense network of tiny blood vessels that deliver oxygen and nutrients to the cells that allow us to see.
In people with diabetes, high blood sugar can gradually weaken these delicate blood vessels. Over time, the vessels may leak, become blocked, or grow abnormally. This process disrupts the normal supply of oxygen to the retina and can eventually lead to vision problems or blindness.
Until now, scientists believed that many of the harmful changes in diabetic retinopathy were mainly driven by a protein called VEGF, which stimulates abnormal blood vessel growth. Several current treatments target VEGF. These therapies can help slow the disease, but they usually work only after damage has already begun, and they do not help all patients.
The new research suggests that another protein may start the damage much earlier. In experiments using mice with diabetes, the scientists discovered that LRG1 causes cells around the smallest blood vessels in the retina to tighten too much.
These cells normally help control blood flow in tiny vessels called capillaries. However, when LRG1 levels increase, the cells squeeze the vessels too strongly. This constriction reduces the amount of oxygen that reaches the retina.
When oxygen levels drop, the retina becomes stressed. This can trigger a chain reaction of biological events that eventually leads to the well-known signs of diabetic retinopathy, such as leaking blood vessels and abnormal new vessel growth.
To test whether blocking this protein could prevent damage, the researchers used methods to stop LRG1 from acting in diabetic mice. The results were striking. When LRG1 was blocked, the early damage to the retina did not occur, and the normal function of the eye was preserved. This suggests that the protein plays a central role in starting the disease process.
According to the lead author, Dr. Giulia De Rossi from the UCL Institute of Ophthalmology, the discovery changes how scientists think about the disease. Instead of focusing mainly on treating damage after it appears, future therapies might be able to stop the disease before it begins to harm vision.
This idea is important because diabetic retinopathy often develops silently. Many patients only notice symptoms such as blurred vision, dark spots, or distorted sight after significant damage has already occurred. At that stage, treatment can slow further deterioration but may not fully restore lost vision.
The discovery of LRG1 as an early trigger suggests that doctors may eventually be able to intervene much earlier in the disease. If a therapy could block the activity of this protein, it might prevent the harmful chain reaction from starting.
The research team has already developed a drug designed to target LRG1. Earlier laboratory studies have shown promising results, and the treatment is currently undergoing further preclinical testing. Scientists hope that human clinical trials could begin in the near future if the research continues to progress successfully.
Interestingly, the researchers believe that blocking LRG1 might help patients at multiple stages of the disease. While the protein appears to trigger early damage, it also continues to play a role in later stages. This means a treatment targeting LRG1 could potentially benefit both people who are just developing diabetic retinopathy and those who already have more advanced disease.
The discovery is the result of several years of work by scientists studying how LRG1 affects blood vessels in the eye. Professors John Greenwood and Stephen Moss from the UCL Institute of Ophthalmology were among the first researchers to identify the protein’s role in eye disease. In 2019 they helped create a biotechnology company called Senya Therapeutics to develop medicines that target LRG1.
Experts involved in supporting the research say the findings are especially encouraging because diabetic retinopathy remains a major global health challenge. Nearly one third of adults living with diabetes show signs of retinal damage, and the number of people with diabetes continues to grow worldwide.
From a scientific perspective, the study provides an important new understanding of how diabetic eye disease begins. Instead of viewing the condition only as a late-stage problem involving abnormal blood vessel growth, the research highlights earlier changes in blood flow and oxygen delivery in the retina.
However, it is important to note that the experiments were conducted mainly in animal models. While these results are promising, further research in humans will be needed to confirm that the same biological process occurs in people. Clinical trials will also be necessary to test whether LRG1-targeting treatments are safe and effective for patients.
Even so, the findings represent a significant step forward. By identifying a possible trigger for the earliest stages of diabetic retinopathy, scientists may have found a new way to protect vision before serious damage occurs. If future studies confirm the results, treatments that block LRG1 could potentially prevent blindness in millions of people living with diabetes.
In summary, the study offers strong evidence that LRG1 is an early driver of diabetic retinal damage and may represent a powerful new target for therapy.
The discovery also highlights the importance of early biological research in uncovering hidden mechanisms of disease. While more work remains before a new treatment reaches patients, the findings open an exciting path toward preventing vision loss rather than simply managing it after the fact.
If you care about diabetes, please read studies about 5 vitamins that may prevent complication in diabetes, and how to manage high blood pressure and diabetes with healthy foods.
For more health information, please see recent studies about vitamin D and type2 diabetes, and to people with type 2 diabetes, some fruits are better than others.
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