Antiangiogenic cytokines as potential new therapeutic targets for resveratrol in diabetic retinopathy

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Term Occurence Count Dictionary
Insulin 1 endocrinologydiseasesdrugs
dexamethasone 2 endocrinologydiseasesdrugs
diabetic retinopathy 15 endocrinologydiseases
hyperglycemia 9 endocrinologydiseases

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Select Drug Character Offset Drug Term Instance
Insulin 34064 growth factor-βControls proliferation and cellular differentiationAlters growth factor’s balance Insulin -like growth factor-IPromotes cellular growth and insulin-like metabolic effectsAutocrine/paracrine regulation
dexamethasone 6266 frequently used first-line therapy agent for DME.[14]–[16] Intravitreal steroid implants (such as dexamethasone or fluocinolone acetonide) exert their anti-inflammatory action, with minimum side effects, and have
dexamethasone 6963 practice, as well as in earlier DME development stages.[17] Refractory cases of DME to ranibizumab or dexamethasone could be switched to aflibercept. Studies comparing the two agents (ranibizumab and aflibercept) offer
Select Disease Character Offset Disease Term Instance
diabetic retinopathy 124 Development and TherapyAntiangiogenic cytokines as potential new therapeutic targets for resveratrol in diabetic retinopathy Mihaela PopescuCătălina BogdanAdela PinteaDumitriţa RuginăCorina Ionescu1Department of Biochemistry,
diabetic retinopathy 949 disorders it can cause. Active research in the field of diabetes includes microvascular complications in diabetic retinopathy (DR). Disturbances in the balance of pro-angiogenesis and anti-angiogenesis factors can lead to the
diabetic retinopathy 3385 important cause of mortality. One of the leading causes of blindness in adults aged 20–74 years is diabetic retinopathy (DR).[2] In DR, progressive damage to the retina occurs when fragile blood vessels break, causing swelling
diabetic retinopathy 5844 of DR, and the risk increases with the severity of the disease: 3% cases with mild nonproliferative diabetic retinopathy (NPDR), 38% cases with moderate-to-severe NPDR, and 71% cases with PDR.[13] Intravitreal VEGF inhibitors
diabetic retinopathy 29231 complications.Figure 1The main mechanisms of hyperglycemia-induced damage considered responsible for the occurrence of diabetic retinopathy : increased polyol pathway flux, increased AGEs formation, increased hexosamine pathway flux, and activation
diabetic retinopathy 29464 PKC.Notes: Adapted from Safi SZ, Qvist R, Kumar S, Batumalaie K, Ismail IS. Molecular mecha nisms of diabetic retinopathy , general preventive strategies, and novel therapeutic targets. Biomed Res Int. 2014;2014:801269. Copyright
diabetic retinopathy 30039 cofactor).Notes: Adapted from Safi SZ, Qvist R, Kumar S, Batumalaie K, Ismail IS. Molecular mecha nisms of diabetic retinopathy , general preventive strategies, and novel therapeutic targets. Biomed Res Int. 2014;2014:801269. Copyright
diabetic retinopathy 30750 impairments.Notes: Adapted from Safi SZ, Qvist R, Kumar S, Batumalaie K, Ismail IS. Molecular mecha nisms of diabetic retinopathy , general preventive strategies, and novel therapeutic targets. Biomed Res Int. 2014;2014:801269. Copyright
diabetic retinopathy 31943 pathogenesis of DR.Note: Original figure; adapted from data from Giacco and Brownlee.[41]Abbreviations: DR, diabetic retinopathy ; F-6-P, fructose-6-phosphate; G-6-P, glucose-6-phosphate; GFAT, glutamine–fructose-6-phosphate aminotransferase;
diabetic retinopathy 32339 factor-beta 1.Figure 6Schematic presentation of the contribution of PKC activation to the development of diabetic retinopathy .Note: Original figure; adapted from data from Geraldes and King.[43]Abbreviations: DAG, diacylglycerol;
diabetic retinopathy 32690 factors.Figure 7Schematic presentation of a possible mechanism of action for resveratrol in the development of diabetic retinopathy .Abbreviations: AGEs, advanced glycation end-products; BRB, blood–retinal barrier; MMPs, matrix metalloproteinases;
diabetic retinopathy 33643 https://www.rcophth.ac.uk/wp-content/uploads/2014/12/2013-SCI-301-FINAL-DR-GUIDELINES-DEC-2012-updated-July-2013.pdf. © The Royal College of Ophthalmologists 2012. All rights reserved.[24]Abbreviations: DR, diabetic retinopathy ; IRMA, intraretinal microvascular abnormalities; NPDR, nonproliferative diabetic retinopathy; PDR, proliferative
diabetic retinopathy 33736 reserved.[24]Abbreviations: DR, diabetic retinopathy; IRMA, intraretinal microvascular abnormalities; NPDR, nonproliferative diabetic retinopathy ; PDR, proliferative diabetic retinopathy.Table 2Proteins secreted from RPE cellsCytokines secreted by
diabetic retinopathy 33777 intraretinal microvascular abnormalities; NPDR, nonproliferative diabetic retinopathy; PDR, proliferative diabetic retinopathy .Table 2Proteins secreted from RPE cellsCytokines secreted by RPEFunctionsRole in DRVEGFProinflammatory
diabetic retinopathy 35034 represent a source of neural regenerationNote: Data adapted from Weight et al.[58]Abbreviations: DR, diabetic retinopathy ; MAPK, mitogen-activated protein kinase; NF-κB, nuclear factor-κB; PI3K, phosphoinositide 3-kinase;
hyperglycemia 9546 DR.[29]Biochemical mechanisms involved in DRDiabetes, in all its forms, is characterized mainly by hyperglycemia . During its course, the development of micro-vascular pathology is likely. Figure 1 shows the four main
hyperglycemia 9678 course, the development of micro-vascular pathology is likely. Figure 1 shows the four main mechanisms of hyperglycemia -induced damage that are considered responsible for the occurrence of DR: increased polyol pathway flux,
hyperglycemia 11620 increase in NADH/NAD+ mimics hypoxia in the tissue (Figure 3).[31],[32]Increased AGEs formationProlonged hyperglycemia amplifies certain physiological nonenzymatic processes, resulting in the formation of a complex and
hyperglycemia 12251 concentrations in diabetic patients in retinal vessels, in vitreous tissues, and in other tissues affected by hyperglycemia .[34],[35] There are three general mechanisms through which AGEs target cells: modification of intracellular
hyperglycemia 13369 production and influencing retinal capillary leukocyte adherence.[40]Increased hexosamine pathway fluxThis hyperglycemia -induced pathway impacts the development of diabetic complications. In its glycolytic pathway, glucose
hyperglycemia 14209 (PAI-1), involved in cell differentiation, growth, and apoptosis.[31],[41] Through the hexosamine pathway, hyperglycemia induces changes in gene expression and protein function, that contribute to the pathogenesis of DR (Figure
hyperglycemia 14606 PKC-ε, PKC-η/l, and PKC-θ), and atypical (PKCζ and PKCλ/ι).[42] Studies showed that intracellular hyperglycemia increases de novo diacylglycerol synthesis, a lipid second messenger that activates the classical PKC
hyperglycemia 15020 through a mechanism unrelated to lipid second messengers[46] through mitochondrial super-oxide induced by hyperglycemia .[47] PKC activation alters the bioavailability of nitric oxide, affects VEGF expression (by decreasing
hyperglycemia 29157 specific tissues that can protect our eyes from diabetic complications.Figure 1The main mechanisms of hyperglycemia -induced damage considered responsible for the occurrence of diabetic retinopathy: increased polyol pathway

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