Endothelial Dysfunction in Diabetic Retinopathy

Abstract

Diabetic retinopathy (DR) is a diabetic complication which affects retinal function and results in severe loss of vision and relevant retinal diseases. Retinal vascular dysfunction caused by multifactors, such as advanced glycosylation end products and receptors, pro-inflammatory cytokines and chemokines, proliferator-activated receptor-γ disruption, growth factors, oxidative stress, and microRNA. These factors promote retinal endothelial dysfunction, which results in the development of DR. In this review, we summarize the contributors in the pathophysiology of DR for a better understanding of the molecular and cellular mechanism in the development of DR with a special emphasis on retinal endothelial dysfunction.

Keywords: diabetes; diabetic retinopathy; endothelial cells; endothelial dysfunction; signaling pathways.

Figure 1

A schematic model of interaction networks mediated by glycosylation end products (AGE) that contributes to blood retinal (BRB) leakage in diabetic retinopathy.

Figure 2

A schematic model of interaction networks mediated by proliferator-activated receptor-γ (PPARγ) disruption that contributes to blood retinal (BRB) leakage in diabetic retinopathy.

Figure 3

A schematic model of interaction networks mediated by inflammation that contributes to blood retinal barrier (BRB) leakage in diabetic retinopathy.

Figure 4

A schematic model of interaction networks mediated by miRNAs that contributes to blood retinal (BRB) leakage in diabetic retinopathy.