Blocking key enzyme prevents development of retinopathy in mice

A six-year study of retinal inflammation in diabetic retinopathy has brought to light the actions of an enzyme that affects the development of the disease in mice.
Retinopathy is a complication of diabetes caused by damage to small blood vessels in the retina which is initiated by prolonged high blood glucose levels.
The new study, spearheaded by Goethe University scientists, in Germany, is focused on understanding a common feature of diabetic retinopathy: retinal vascular inflammation.
Retinal inflammation leads to structural changes affecting blood flow and oxygen supply in retinal capillaries, which increases the risk for proliferative retinopathy and blindness.
The researchers explored ways to increase tissue levels of compounds with anti-inflammatory effects in order to halt these processes in the retina and preserve vision.
These compounds are known as fatty acid epoxides, and their level can be modulated by blocking an enzyme called soluble epoxide hydrolase (sEH).
The sEH enzyme breaks down fatty acid epoxides into harmful compounds that promote the loss of cells protecting the lining of retinal capillaries.
In humans, the inhibition of sEH was previously studied for the treatment of hypertension and heart disease but it had not yet been examined in retinal disease.
Earlier research did, however, suggest that the severity of retinopathy in humans is associated with a higher expression of sEH in the retina.
In the current study, the research team demonstrated how sEH can damage the retina in mice with diabetes and animals that overproduce sEH.
The research team was able to develop an inhibitor to the enzymen, which prevented the development of retinopathy in the mice with diabetes. Blocking sEH in humans could reduce inflammation and vascular injury in the retina too, according to the researchers.
Overall, these findings suggest that developing new inhibitor drugs aimed at blocking this enzyme could help prevent or treat diabetic retinopathy.
The findings were published in the journal Nature.