Role of Inflammation in Diabetic Retinopathy

Abstract

Diabetic retinopathy is a common complication of diabetes and remains the leading cause of blindness among the working-age population. For decades, diabetic retinopathy was considered only a microvascular complication, but the retinal microvasculature is intimately associated with and governed by neurons and glia, which are affected even prior to clinically detectable vascular lesions. While progress has been made to improve the vascular alterations, there is still no treatment to counteract the early neuro-glial perturbations in diabetic retinopathy. Diabetes is a complex metabolic disorder, characterized by chronic hyperglycemia along with dyslipidemia, hypoinsulinemia and hypertension. Increasing evidence points to inflammation as one key player in diabetes-associated retinal perturbations, however, the exact underlying molecular mechanisms are not yet fully understood. Interlinked molecular pathways, such as oxidative stress, formation of advanced glycation end-products and increased expression of vascular endothelial growth factor have received a lot of attention as they all contribute to the inflammatory response. In the current review, we focus on the involvement of inflammation in the pathophysiology of diabetic retinopathy with special emphasis on the functional relationships between glial cells and neurons. Finally, we summarize recent advances using novel targets to inhibit inflammation in diabetic retinopathy.

Hyperglycemia‐induced ubiquitination and degradation of β‐catenin with the loss of platelet endothelial cell adhesion molecule‐1 in retinal endothelial cells

“…Retinal vascular endothelial cells create the barrier needed to limit plasma leakage into the retinal neuronal tissue. However, in pathophysiological conditions, such as the inflammatory response during DR, the intercellular junction may break down as a response to cytokines, such as TNF‐α or histamine, leading to the extravasation of inflammatory cells, proteins, and fluid into the extravascular space . Under normal circumstances, this process is reversible due to the ability of the intercellular junction proteins, such as VE‐cadherin, and its adaptor protein β‐catenin, to restore the barrier function .…”

Eriodictyol inhibits high glucose‐induced oxidative stress and inflammation in retinal ganglial cells

“…A, Cell apoptosis was assessed using ELISA to detect cytosolic DNA-histone complex generated during apoptotic DNA fragmentation. 17 Taken together, oxidative stress and inflammation are considered as critical contributors to the development of DR. Increasing evidence points to specific mechanism-based strategies for preventing DR by targeting both oxidative stress and inflammatory. *P < 0.05 versus control cells; # P < 0.05 versus HG-stimulated cells.…”

Effect of basal insulin supplement therapy on diabetic retinopathy in short‐duration type 2 diabetes: A one‐year randomized parallel‐group trial

“…Inflammation is a major pathogenic factor associated with DR . Both general hyperglycemia and GV can induce and enhance inflammation .…”