Inflammation and diabetic retinal microvascular complications

Abstract

Diabetic retinopathy (DR) is one of the most common complications of diabetes and is a leading cause of blindness in people of the working age in Western countries. A major pathology of DR is microvascular complications such as non-perfused vessels, microaneurysms, dot/blot hemorrhages, cotton-wool spots, venous beading, vascular loops, vascular leakage and neovascularization. Multiple mechanisms are involved in these alternations. This review will focus on the role of inflammation in diabetic retinal microvascular complications and discuss the potential therapies by targeting inflammation.

Keywords: Diabetic retinopathy; inflammation; microvascular complications.

Figure 1

Cascade of events that contribute to the inflammatory response in diabetic retinopathy. Hyperglycemia induces formation of advanced glycation end products, generation of reactive oxygen species from multiple sources, mainly nicotinamide adenine dinucleotide phosphate oxidase and mitochondrial electron transport chain, and dysregulation of nitric oxide synthase (NOS) pathway. These changes activate NF-kB and, in turn, upregulation of cytokines, chemokines and iNOS. This leads to upregulation of adhesion molecules and subsequent leukocyte/endothelial interaction