Diabetic retinopathy is the number one cause of new blindness in most industrialized countries. The risk of its development is directly related to the degree and duration of elevated blood glucose. Thus, the incidence of retinopathy is 25% when diabetes mellitus has been present for five to ten years, and it rises to 70% to 90% in subjects who have been diabetic for more than 10 years.

The earliest clinically detectable signs are microaneurysms of the capillary wall, small intraretinal hemorrhages, and leakage of plasma proteins from the abnormal capillaries. This phase is followed by a more extensive capillary damage, more intraretinal hemorrhages, and leakage of fluid from the capillaries around the macula. The macula is the region of the retina responsible for maximal visual acuity, and, therefore, the presence of edema in this region leads to a significant loss of vision.

The last stage of retinal disease is characterized by the formation of new blood vessels (neovascularization), fibrovascular membranes, hemorrhage into the vitreous, and fibrous bands between the vitreous and the retina leading to tractional retinal detachment. Current methods of treatment include control of blood glucose and pressure, laser photocoagulation, and vitrectomy.

The concentration of CTGF in ocular fluids obtained from patients with diabetic retinopathy undergoing eye surgery is correlated with the degree of intraocular fibrosis and neovascularization. A correlation between the intraocular levels of Vascular Endothelial Growth Factor (VEGF) and CTGF has been reported, raising the possibility that the pathogenic effects of VEGF in the eye may be mediated by CTGF. In vitro experiments conducted in retinal vascular cells support such a possibility. CTGF may be an important causal factor in ocular fibrosis and neovascularization and therefore represents a suitable therapeutic target for the prevention of sight-threatening vitreoretinal scarring.