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Finally, novel drug targets including components of the kinin–kallikrein system and emerging treatments such as anti-HPTP (human protein tyrosine phosphatase) β antibodies are discussed.Recognition of non-VEGF contributions to disease pathogenesis may lead to novel therapeutics to enhance existing treatments for patients who do not respond to anti-VEGF therapies.Like the brain, formation of these specialized endothelial cells requires interaction with glia and pericytes and recent studies have identified the contribution of Norrin signaling from glia as required for development and maintenance of the BRB .The glia and pericytes provide endothelial support and protection, and their loss results in increased endothelial permeability .
Approximately 60% of individuals with type 2 diabetes and nearly all individuals with type 1 diabetes show at least some signs of DR [1,2].
Further, the retina is immune-privileged or at a minimum, restricted .
The blood-retinal barrier (BRB) describes the unique make-up of the retinal vasculature and RPE cells that tightly control the flux of fluid and blood borne material into and out of the retina and confer immunoprivilege.
The current worldwide estimate of diabetic patients with any form of DR is 92.6 million, including 17.2 million with the more serious proliferative form of DR, 20.6 million with diabetic macular edema (DME) and a total of 28.4 million people with DR that is considered to be a threat to vision .
In the US, it is projected that by the year 2050 up to one third of the total adult population could have diabetes, leading to a vast increase in cases of DR .
The phenotypes of TJ protein gene deletion include embryonic lethality for ZO-1 , ZO-2 , and claudin-1 , aberrant permeability regulation (claudin 2  and claudin 10 ), increased permeability (claudin 5  and claudin 18 ), or various blood–barrier related pathologies (occludin [33,34]).