Abstract

Diabetic retinopathy is a major cause of vision loss in the working population of developed countries. Laser therapy constitutes a proven treatment for diabetic macular edema and proliferative diabetic retinopathy, but often at the cost of functional retina and visual performance. This article focuses on some recent advances that have improved our understanding of pathogenic mechanisms underlying the initiation and progression of diabetic retinopathy, which may have an impact on the development of new pharmacotherapies for this condition. In particular, the role of large conductance Ca2+-activated K+ channels in mediating early changes in retinal blood flow, the involvement of extracellular carbonic anhydrase in the etiology of diabetic macular edema, and the possible contribution of circulating endothelial progenitor cells to defective vascular repair in the diabetic retina, is emphasized.

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