Sweet Stress: Coping With Vascular Dysfunction in Diabetic Retinopathy

Figures

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  FIGURE 1. Schematic cross-section showing the retinal blood vessels lining the inner surface of the retina. Three capillary plexuses are embedded among retinal neurons: the superficial layer lies within the inner nerve fiber layer (NFL) with branches extending into the ganglion cell layer (GCL), while the intermediate and deep capillary plexuses align along each sides of the inner nuclear layer (INL). ONL, outer nuclear layer. IPL, inner nuclear layer; OPL, outer plexiform layer.

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  FIGURE 2. Biochemical pathways leading to diabetic retinopathy. Chronic hyperglycemia promotes the increase in ROS formation, originating in the mitochondria or produced by Nox, and also activates many metabolic pathways, including PKC, polyol pathway, AGEs, and the hexosamine pathway, as well as the production of inflammatory mediators. Oxidative stress damages mitochondrial DNA resulting in a decline in mitochondrial function, which accelerates cell apoptosis, contributing to the development of diabetic retinopathy.

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  FIGURE 3. Processes leading to BRB breakdown in diabetic retinopathy. During the development of diabetic retinopathy, increased production of ROS leads to increased expression of intercellular adhesion molecules in endothelial cells, and consequently increased leukocyte adhesion. Concurrently, astrocytes, Müller cells, and microglia become activated, promoting cytokine release, and pericytes surrounding endothelial cells die by apoptosis. Moreover, vascular ROS and inflammatory mediators that are released by inflammatory cells affect endothelial tight junctions leading to increased BRB permeability.