Abstract
There is a growing body of evidence that advanced glycation end product-receptor(AGE-RAGE) interaction elicits oxidative stress generation, thus indicating that it is involved in the pathogenesis of diabetic retinopathy. Inhibition of AGE formation or blockade of the downstream RAGE signaling is a promising therapeutic strategy for treatment of patients with diabetic retinopathy.
MeSH terms
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Animals
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Apoptosis
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Diabetic Retinopathy / etiology*
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Diabetic Retinopathy / therapy
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Endothelial Cells
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Epoprostenol / biosynthesis
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Eye Proteins / physiology
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Glycation End Products, Advanced* / physiology
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Humans
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Microcirculation / cytology
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Neovascularization, Pathologic
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Nerve Growth Factors / physiology
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Oxidative Stress
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Receptor for Advanced Glycation End Products
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Receptors, Immunologic / physiology
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Retinal Vein Occlusion / etiology
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Retinal Vessels / cytology
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Serpins / physiology
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Signal Transduction / physiology
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Vascular Endothelial Growth Factor A / metabolism
Substances
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Eye Proteins
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Glycation End Products, Advanced
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Nerve Growth Factors
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Receptor for Advanced Glycation End Products
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Receptors, Immunologic
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Serpins
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Vascular Endothelial Growth Factor A
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pigment epithelium-derived factor
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Epoprostenol