Breakdown of the inner endothelial blood-retinal barrier (BRB), as occurs in diabetic retinopathy, age-related macular degeneration, retinal vein occlusions, uveitis and other chronic retinal diseases, results
in vasogenic edema and neural tissue damage, causing loss of vision. The central mechanism of
altered BRB function is a change in the permeability characteristics of retinal endothelial cells caused by
elevated levels of growth factors, cytokines, advanced glycation end products, inflammation, hyperglycemia
and loss of pericytes. Subsequently, paracellular but also transcellular transport across the retinal
vascular wall increases via opening of endothelial intercellular junctions and qualitative and quantitative
changes in endothelial caveolar transcellular transport, respectively. Functional changes in pericytes and
astrocytes, as well as structural changes in the composition of the endothelial glycocalyx and the basal
lamina around BRB endothelium further facilitate BRB leakage.
The inner blood-retinal barrier (BRB) is made up by the neurovascular unit, consisting of endothelial cells, pericytes and glial cells. The BRB maintains homeostasis of the neural retina, but in pathological eye conditions the neurovascular unit is often disrupted, causing BRB loss.
Expression patterns of endothelial permeability pathways in the development of the blood-retinal barrier in mice.