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8611662 
Journal Article 
Oxidative stress and diabetic retinopathy: Molecular mechanisms, pathogenetic role and therapeutic implications 
Kang, QZ; Yang, CX 
2020 
1 
Redox Biology
ISSN: 2213-2317 
37 
17 
English 
33248932 
WOS:000604974200003 
Oxidative stress, a cytopathic outcome of excessive generation of ROS and the repression of antioxidant defense system for ROS elimination, is involved in the pathogenesis of multiple diseases, including diabetes and its complications. Retinopathy, a microvascular complication of diabetes, is the primary cause of acquired blindness in diabetic patients. Oxidative stress has been verified as one critical contributor to the pathogenesis of diabetic retinopathy. Oxidative stress can both contribute to and result from the metabolic abnormalities induced by hyperglycemia, mainly including the increased flux of the polyol pathway and hexosamine pathway, the hyperactivation of protein kinase C (PKC) isoforms, and the accumulation of advanced glycation end products (AGEs). Moreover, the repression of the antioxidant defense system by hyperglycemia-mediated epigenetic modification also leads to the imbalance between the scavenging and production of ROS. Excessive accumulation of ROS induces mitochondrial damage, cellular apoptosis, inflammation, lipid peroxidation, and structural and functional alterations in retina. Therefore, it is important to understand and elucidate the oxidative stress-related mechanisms underlying the progress of diabetic retinopathy. In addition, the abnormalities correlated with oxidative stress provide multiple potential therapeutic targets to develop safe and effective treatments for diabetic retinopathy. Here, we also summarized the main antioxidant therapeutic strategies to control this disease. 
Oxidative stress; Diabetic retinopathy; Reactive oxygen species; Dysmetabolism; Epigenetic modification; Antioxidant therapeutics; glycation end-products; nf-kappa-b; protein-kinase-c; endothelial; growth-factor; retinal metabolic abnormalities; antioxidant-responsive; element; nitric-oxide synthase; 3 major pathways; epigenetic; modifications; nadph oxidase; Biochemistry & Molecular Biology