Abstract
This article evaluates the current knowledge of the molecular mechanisms by which diabetes ocular and systemic inflammation induce breakdown of the blood-retinal barrier resulting in macular edema. We also summarize the relationship between molecular targets and the use of therapeutic inhibitors in preclinical studies and clinical trials. Further studies are needed to understand the regulation of normal blood-retinal barrier physiology and the relationship between events in animal models of diabetic retinopathy and humans with diabetes.
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