A new study has found that a naturally occurring enzyme has the ability to tamp down inflammation and may protect the eyes in diabetes and premature birth.
The study, conducted by researchers at Children’s Hospital of Philadelphia (CHOP) and the University of Pennsylvania, found that the enzyme, called Dicer, can prevent the damaging effects of inflammation in the body.
Dicer is a protein that is produced by the body in response to inflammation. It is known to play a role in regulating the inflammatory response.
The researchers found that when Dicer is absent, or when it is not functioning properly, the body is unable to properly regulate the inflammatory response. This can lead to the development of chronic diseases, such as diabetes and premature birth.
The study found that when Dicer is present, it is able to prevent the damaging effects of inflammation.
“We found that Dicer is a powerful regulator of inflammation and its absence leads to a heightened inflammatory response,” said senior author and CHOP researcher, Dr. Jason Christie.
“Dicer has the ability to shut down the inflammatory response, preventing the damaging effects of inflammation.”
The study’s findings are published in the journal Nature Medicine.
“Our findings suggest that Dicer may be a novel therapeutic target for the treatment of chronic inflammatory diseases, such as diabetes and premature birth,” said Dr. Christie.
The study’s findings are based on research conducted in mouse models. The next step is to conduct clinical trials in humans to confirm the findings.
The researchers are hopeful that the findings of the study will lead to the development of new and more effective treatments for chronic inflammatory diseases.
According to a new study, a potent enzyme that inhibits inflammation could help to protect the eyes in diabetes and other conditions.
The findings, published in the journal Nature Medicine, suggest that the enzyme, called interleukin-1 receptor-associated kinase 4 (IRAK4), could be a potential therapeutic target for treating diabetes-related eye diseases.
IRAK4 is a key component of the innate immune response, and its activity is known to be upregulated in response to inflammation.
Previous studies have shown that IRAK4 inhibits the activity of pro-inflammatory cytokines, and that it is highly expressed in the eye.
In the new study, the research team set out to determine whether IRAK4 could protect against diabetes-related damage to the retina.
They generated a mouse model of diabetes by injecting them with streptozotocin, and then treated the mice with a small molecule inhibitor of IRAK4.
The results showed that the IRAK4 inhibitor protected the retina from damage, and also reduced levels of the pro-inflammatory cytokine interleukin-6 in the eye.
In another experiment, the team found that IRAK4-deficient mice were protected from diabetes-related damage to the retina.
“Our findings suggest that IRAK4 is a key player in the pathogenesis of diabetic retinopathy, and that targeting this enzyme could be a potential therapeutic strategy for this disease,” says study senior author Dr. Miguel Soares, of Harvard Medical School and Massachusetts General Hospital.
The team plans to further investigate the therapeutic potential of IRAK4 inhibitors in animal models of diabetic retinopathy and other eye diseases.