New target for retinopathy therapy discovered

A variant form of vascular endothelial growth factor (VEGF) has been discovered to be responsible for the inflammation and altered retinal vascularization that occurs in conditions such as diabetic retinopathy (DR), according to an announcement made at the European meeting on Vascular Biology and Medicine in Bristol, England.

Professor David Shima from University College London, UK and co-workers discovered that, although blood vessels in the ischaemic retina re-grow, they do so in a disorganized fashion, forming clumps rather than a fine, mesh-like network. The researchers characterized the VEGF activity responsible for the abnormal response and identified an isoform, VEGF 164, which drives ocular neovascularization, vascular permeability and an inflammatory reaction.

When VEGF 164 was inhibited, either genetically or pharmaceutically, pathological neovascularization was also inhibited and blood vessels were able to form normally. Further investigation found a specific region within VEGF 164 that is a major cause of DR inflammation.

Although this inflammatory function of VEGF 164 represents a target for DR treatment, VEGF has a second, beneficial role in protecting neurons from ischaemic death, so eliminating it completely could trigger unwanted consequences.