Diabetic Retinopathy: Vascular and Inflammatory Disease

Abstract

Diabetic retinopathy (DR) is the leading cause of visual impairment in the working-age population of the Western world. The pathogenesis of DR is complex and several vascular, inflammatory, and neuronal mechanisms are involved. Inflammation mediates structural and molecular alterations associated with DR. However, the molecular mechanisms underlying the inflammatory pathways associated with DR are not completely characterized. Previous studies indicate that tissue hypoxia and dysregulation of immune responses associated with diabetes mellitus can induce increased expression of numerous vitreous mediators responsible for DR development. Thus, analysis of vitreous humor obtained from diabetic patients has made it possible to identify some of the mediators (cytokines, chemokines, and other factors) responsible for DR pathogenesis. Further studies are needed to better understand the relationship between inflammation and DR. Herein the main vitreous-related factors triggering the occurrence of retinal complication in diabetes are highlighted.

Figure 1

The role of innate immunity in diabetic retinopathy and type 2 diabetes mellitus. In patients with type 2 diabetes and diabetic retinopathy, innate immune markers and proinflammatory cytokines, including IL-1β, IL-6, IL-8, TNF-α, and prostaglandin E2, are upregulated. The cytokines then enter systemic circulation and contribute to the diabetic pathology by increasing insulin resistance and by elevating blood glucose levels.

Figure 2

Role of vitreous mediators in DR progression. In DR, several inflammatory vitreous mediators are upregulated and induce anatomical changes in the retinal tissue. The structural changes enhance retinal tissue degeneration and mediate pathogenesis of DR.