Abstract
The earliest and most significant change in diabetic retinopathy (DR) is blood-retinal barrier (BRB) dysfunction, followed by two main pathologies that may cause severe visual impairment: Diabetic Macular Edema (DME) and Proliferative Diabetic Retinopathy (PDR). The pathological hallmarks of BRB dysfunction include loss of tight junction integrity, VEGF- and AGE-induced damage, oxidative stress, and inflammatory changes. Recently, several BRB protective factors have been reported. Our aim is to give a review of those protective factors and discuss new potential therapeutic targets for DR.
MeSH terms
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Animals
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Blood-Retinal Barrier / drug effects
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Blood-Retinal Barrier / pathology
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Blood-Retinal Barrier / physiopathology*
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Diabetic Retinopathy / etiology
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Diabetic Retinopathy / physiopathology*
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Diabetic Retinopathy / prevention & control*
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Erythropoietin / pharmacology
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Fenofibrate / analogs & derivatives
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Fenofibrate / pharmacology
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Humans
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Insulin-Like Growth Factor Binding Protein 3 / physiology
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Macular Edema / complications
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Macular Edema / pathology
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Macular Edema / physiopathology
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Protective Factors
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Pyrazines / pharmacology
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Sitagliptin Phosphate
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Triazoles / pharmacology
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Vascular Endothelial Growth Factor A / antagonists & inhibitors
Substances
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IGFBP3 protein, human
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Insulin-Like Growth Factor Binding Protein 3
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Pyrazines
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Triazoles
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VEGFA protein, human
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Vascular Endothelial Growth Factor A
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Erythropoietin
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fenofibric acid
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Sitagliptin Phosphate
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Fenofibrate