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.
Acknowledgements
This work was supported by The Juvenile Diabetes Research Foundation, The Wellcome Trust and Fight for Sight, UK.
Financial & competing interests disclosure
The authors have no relevant affiliations or financial involvement with any organization or entity with a financial interest in or financial conflict with the subject matter or materials discussed in the manuscript. This includes employment, consultancies, honoraria, stock ownership or options, expert testimony, grants or patents received or pending, or royalties.
No writing assistance was utilized in the production of this manuscript.