Oxidative Stress-Related Mechanisms and Antioxidant Therapy in Diabetic Retinopathy

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diabetic retinopathy 1 endocrinologydiseases
fenofibrate 1 endocrinologydiseasesdrugs
hyperglycemia 15 endocrinologydiseases
simvastatin 2 endocrinologydiseasesdrugs

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fenofibrate 37796 retinal SIRT1 pathway and protects the retina from diabetic insult [[156]]. Moreover, resveratrol and fenofibrate also have a protective effect on DR via SIRT1-related pathways [[118], [157]].6. ConclusionsDR is a
simvastatin 18799 H-Ras in diabetes is mediated by its translocation to the plasma membrane, which can be prevented by simvastatin , an inhibitor that blocks the membrane translocation of H-Ras [[72]]. Evidence suggests that activated
simvastatin 42031 translocates from the cytosol to the membrane and H-Ras binds to GTP. The former can be inhibited by simvastatin ; the latter can be activated by guanine nucleotide exchange factor (GNEF). After that, Raf-1 also can
Select Disease Character Offset Disease Term Instance
diabetic retinopathy 39962 which could produce ROS and result in oxidative stress.Figure 2The mechanisms of oxidative stress and diabetic retinopathy . BRB, blood-retinal barrier; ET-1, endothelin-1; NADPH, nicotinamide adenine dinnucleotide phosphate;
hyperglycemia 2476 this period [[3]].The development of DR is associated with sustained metabolic disorders caused by hyperglycemia and increased levels of inflammatory cytokines in the blood. Systemic inflammation caused by these metabolic
hyperglycemia 3480 thought to be one of the crucial factors in the pathogenesis of DR. Abnormal metabolism induced by hyperglycemia can result in the overproduction of free radicals such as hydroxyl and superoxide radicals, which are
hyperglycemia 3802 damages the tissue in and around retinal vessels, ultimately resulting in DR. It is well known that hyperglycemia can cause vascular damage through four classical mechanisms: increased polyol pathway flux; increased
hyperglycemia 7728 most metabolically active tissue in the body and is therefore easily affected by diabetes. Sustained hyperglycemia damages the microvasculature of the retina resulting in hemodynamic changes, thickening of the basement
hyperglycemia 9947 of hypoxia during DR, thereby protecting the microvasculature from pathogenic change. Furthermore, hyperglycemia -induced endothelial injury can produce reactive nitrogen species through the activation of arginase,
hyperglycemia 13606 modification of Ser/Thr residues by O-linked β-N-acetylglucosamine. A recent study demonstrated that hyperglycemia promotes the GlcNAcylation of NF-κB, which contributes to the death of retinal gangliocytes [[56]].
hyperglycemia 25933 protein-mediated inflammation in high-glucose cultured retinal endothelial cells [[98]]. Moreover, transient hyperglycemia can induce upregulation of NF-κB subunit p65, which acts as an inflammatory mediator in diabetes, via
hyperglycemia 26524 acylation and methylation in monocytes at inflammation- and diabetes-related gene loci can be induced by hyperglycemia [[102], [103]]. Both hyperglycemia and hydrogen peroxide treatment increase the expression of coactivator-associated
hyperglycemia 26559 at inflammation- and diabetes-related gene loci can be induced by hyperglycemia [[102], [103]]. Both hyperglycemia and hydrogen peroxide treatment increase the expression of coactivator-associated arginine methyltransferase
hyperglycemia 32482 analogue of thiamine monophosphate, can protect vascular cells from the metabolic damage induced by hyperglycemia . In diabetic animals, benfotiamine has been shown to inhibit three major ROS production pathways (the
hyperglycemia 33763 stress, also contributes to the development of DR. The overexpression of manganese SOD can decrease the hyperglycemia -induced expression of VEGF mRNA and protein in endothelial cells, and the expression of VEGF and fibronectin
hyperglycemia 37558 targeting specific miRNAs [[9]]. Metformin, which is involved in the SIRT1/LKB1/AMPK pathway, suppresses hyperglycemia stress “memory” in diabetic rats [[155]]. Another research has shown that cocoa enriched with polyphenol
hyperglycemia 38065 oxidative stress plays an important role in its development. In this review, we have demonstrated that hyperglycemia induces a series of metabolic abnormalities in the retina by producing ROS and subsequently initiating
hyperglycemia 40291 endothelial growth factor.Figure 3The activation of the three main protein kinase C (PKC) isoforms induced by hyperglycemia . AGE, advanced glycation end-products; BRB, blood-retinal barrier; DAG, diacylglycerol; eNOS, endothelial
hyperglycemia 41276 important enzyme in glutathione (GSH) synthesis, thus resulting in the decrease of GSH. On the other hand, hyperglycemia facilities methylation of the Keap1 promoter via methyltransferase enzyme Set7/9 (SetD7), which eases

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