Diabetic retinopathy (DR) is the leading cause of acquired blindness, which is one of the most feared complications of diabetes among young adults. The cause of vision loss in DR is complex and remains incompletely understood. One of the earliest changes in the development of retinopathy is break down of blood-retinal barrier (BRB) and the formation of acellular capillaries by unknown mechanism. There is an accumulating body of evidence that demonstrated, chronic low-grade subclinical inflammation and retinal leukocyte stasis are responsible for many of the vascular lesions in DR. In the retina, diabetes induced sustained proinflammatory responses by increasing the production of proinflammatory cytokines, chemokines, and other inflammatory mediators leading to damaged vasculature and neovascularization. An emerging issue in DR research is the focus on the mechanistic link between chronic low-grade inflammation and angiogenesis. Recent evidence has revealed that extracellular high-mobility group box-1 (HMGB1) protein acts as a potent proinflammatory cytokine that triggers inflammation and recruits leukocytes to the site of tissue damage, and exhibits angiogenic effects. The expression of HMGB1 is upregulated in epiretinal membranes and vitreous fluid from patients with proliferative DR and in the diabetic retina. HMGB1 mediates inflammation, breakdown of the BRB, and apoptosis in the diabetic retina. The overall objective of this chapter is to provide the up-to-date literature about the crosstalk between extracellular HMGB1 and DR.
Part of the book: Role of Biomarkers in Medicine