Min K Song, Basil D Roufogalis and Tom H.W Huang
Diabetic retinopathy (DR) is one of the most common complications of diabetes and one of the leading causes of blindness worldwide. DR involves an abnormal pathology of major retinal cells, including retinal pigment epithelium, vascular cells (endothelial cells and pericytes), retinal microglial cells and retinal ganglion cells. The biochemical mechanisms associated with hyperglycemic-induced DR are through multifactorial processes. Peroxisome proliferatoractivated receptor-γ ( PPAR-γ) plays an important role in the pathogenesis of DR by inhibiting diabetes-induced retinal leukostasis and leakage. Despite DR causing eventual blindness, only a few visual or ophthalmic symptoms are observed until visual loss develops. Laser photocoagulation therapy is the most common treatment. However, this therapy may cause retinal damage and scarring. Therefore, early medical interventions and prevention are the current management strategies. The recent advancements in the knowledge of the pathogenic alterations driving ocular damage and vision loss in DR strongly focus on PPAR-γ as a valuable target to control high glucose-induced inflammation and apoptosis. This review provides an analysis of potential involvement of PPAR-γ in various mechanisms and pathways associated with progression of DR.
