The development of diabetic retinopathy is a long slow process affected by hyperglycemia, hypertension, lipid levels and genetics. It is expected that in 20 years' duration nearly all those with diabetes will exhibit diabetic retinopathy. In some patients, it will progress to blindness. While the number of individuals with diabetes increases, our current treatments are only effective at advanced levels of disease. Further, our screening methods to detect those needing treatment are currently not optimal. Early Events in Diabetic Retinopathy and Intervention Strategies covers topics addressing imaging processes currently available in the development of diabetic retinopathy screening. Potential biomarkers, that may be used to identify those at risk and illuminate the new pathways which lead to diabetic retinopathy, are expounded.Go to the book
Part of the book: Early Events in Diabetic Retinopathy and Intervention Strategies
Hyperglycemic conditions and disruptions to glucose-regulating pathways lead to increased formation of highly reactive aldehydes, methylglyoxal and glyoxal, which react with certain arginine and lysine residues in proteins to form advanced glycation end products (AGEs). These AGEs damage the integrity of the retinal vasculature predominantly through two mechanisms: non-receptor-mediated damage, which pertains to the interaction with extracellular matrix and its functional properties, and receptor-mediated damage through AGE interactions with their receptors (RAGE) on pericytes and Muller cells. Damage occurring between AGE and RAGE potentially generates reactive oxygen species, inflammatory cytokines, and growth factors. Both mechanisms result in increased permeability of endothelial tight junctions, and this increased permeability can lead to leaking and eventually ischemia. Once this ischemia becomes significant, neovascularization can occur, the hallmark of proliferative diabetic retinopathy. Current pharmaceutical studies have shown the potential of AGE inhibitors, such as aminoguanidine, in decreasing AGE production, thus minimizing its effects in hyperglycemic conditions. Other pharmaceutical interventions, such as Tanshinone IIA, aim to protect cells from the impacts of AGEs. Future research will not only continue to understand the properties of AGEs and their effects on diabetes and diabetic complications like diabetic retinopathy but will also explore how they impact other diseases.
Part of the book: The Eye and Foot in Diabetes