Scientists are studying the causes of diabetic retinopathy and trying to develop treatments and preventive methods.

An application for an oral medication, ruboxistaurin (Arxxant), was submitted to the U.S. Food and Drug Administration (FDA) in 2006. Clinical trials found that the drug, a protein kinase inhibitor, reduced loss of vision from diabetic retinopathy. If approved, it would be the first oral medication to reduce risk of vision loss in people with diabetes.

Among other treatments being studied:

• Corticosteroids, a class of anti-inflammatory immunosuppressives, may offer hope. One recent clinical trial found that an injected corticosteroid may improve vision in people with diabetic retinopathy. Side effects included increased risk of glaucoma and cataracts but were described as manageable. Also, a corticosteroid approved to treat an inflammatory eye condition called uveitis may improve vision in people with macular edema. This drug is released from a tiny device that is surgically placed or injected into the eye.  This has been done successfully for a number of years but is used off-label, meaning it is not FDA-approved for this use.
  
  
• Retinopathy and other diabetic conditions are a focus of gene therapy, the introduction of normal genes to fill in for malfunctioning ones. Genetic engineers are also studying stem cells as a way to prevent diabetic retinopathy.
  

• Recent research suggests that a cholesterol-reducing drug may reduce the need for laser treatment of diabetic retinopathy, in addition to preventing nonfatal heart attacks.

A study at the University of Florida is offering some hope that scientists eventually may be able to block the development of diabetic retinopathy. Researchers used an antibody to block a protein called SDF-1 and prevented mice from developing blindness when they had a condition similar to diabetic retinopathy. SDF-1 signals blood stem cells to rush to certain areas of the body.

New research is also suggesting a promising direction for treating proliferative retinopathy, which occurs when the retina does not receive enough blood and new, abnormal blood vessels grow on its surface.

Researchers are studying the role of vascular endothelial growth factor (VEGF) and its receptors. VEGF is one of the known substances that cause new vessels to grow on the retinal surface. It is secreted by retina that is damaged by diabetes.

Studies have confirmed that VEGF is elevated in the eye fluids of patients with diabetes and proliferative diabetic retinopathy. Hypoxia – a deficiency in the amount of oxygen that reaches tissues, and a major factor in triggering the growth of abnormal blood vessels – spurs the secretion of VEGF.

Treatments such as laser photocoagulation cause changes to blood vessel circulation, which improves oxygen delivery to the retina. This results in reduced secretion of VEGF and other factors, leading to fewer troublesome new blood vessels.

In addition, chemicals are being developed that block the effect of VEGF. Researchers are focusing on other methods of blocking the formation of VEGF in the eyes, while allowing it to continue elsewhere in the body (such as in the heart and legs, where formation of new blood vessels is beneficial).

Japanese researchers recently found that a hormone called erythropoietin may be even more strongly linked than VEGF to advanced diabetic retinopathy. They suggested that treatment blocking erythropoietin could prevent the abnormal growth of blood vessels (neovascularization).

Oxygen therapy may hold potential as a treatment option. Scientists at the National Eye Institute and Johns Hopkins University found in a small pilot study that diabetic individuals with macular edema experienced decreased swelling in the eyes and, in some cases, sharper vision after inhaling supplemental oxygen for three months.