The cell-matrix interface: a possible target for treating retinal vascular related pathologies.

Retinal vasculature related pathologies account for a large proportion of global blindness. Choroidal neovascularization accompanying age-related macular degeneration is the largest cause of blindness in people over the age of 65 years, proliferative diabetic retinopathy is the main cause of acquired blindness in working adults, and retinopathy of prematurity (ROP) is the leading cause of acquired blindness in children. Given the great success in treating the first category of these conditions with anti-vascular endothelial growth factor (anti-VEGF) therapy, there is understandably considerable interest to employ this strategy to other retinal vascular disorders. Anti-VEGF therapy may not be the optimal course of action, as it may compromise neuronal survival; this is of particular concern when treating ROP where retinal neurogenesis is still not complete. Moreover, retinal neovascularization is preceded by alterations in the vascular wall extracellular matrix with concomitant reduction in mural cell adhesion. This produces vascular instability followed by the pathobiologic process of neovascularization. Thus, stabilizing mural cell-matrix interactions would be a prudent alternative for controlling retinal vascular pathologies. In this review, we will summarize the development of retinal angiogenesis focusing on the role of cell-matrix interaction in each step of the process. Our goal is to identify potential targets for regulating and maintaining normal vascular development and function.