2008
DOI: 10.1016/j.mehy.2007.03.033
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Bioinformatics analysis of diabetic retinopathy using functional protein sequences

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Cited by 12 publications
(9 citation statements)
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“…NO can contribute to vasodilatation, increase local blood flow, and decrease vascular resistance in ocular circulation. Studies on humans and animal models have suggested that eNOS plays an essential role in retinal vascular function and disequilibrium in its production can lead to the development of DR [911]. The presence of eNOS polymorphisms might contribute to a decreased eNOS activity and a reduced NO level and has been reported to be a potential factor in the pathogenesis and development of DR.…”
Section: Introductionmentioning
confidence: 99%
“…NO can contribute to vasodilatation, increase local blood flow, and decrease vascular resistance in ocular circulation. Studies on humans and animal models have suggested that eNOS plays an essential role in retinal vascular function and disequilibrium in its production can lead to the development of DR [911]. The presence of eNOS polymorphisms might contribute to a decreased eNOS activity and a reduced NO level and has been reported to be a potential factor in the pathogenesis and development of DR.…”
Section: Introductionmentioning
confidence: 99%
“…According to Hernandez C, et al, patients suffering with PDR showed intravitreous cortistatin levels low when compared to non-diabetic patients and higher cortistatin levels in vitreous fluid than in the plasma. No plasma and vitreous cortistatin concentrations relationship suggests a possible role in retinal homeostasis [23,24]. Generally increase in hyperglycemia increases the activity of aldose reductase which in turns set off a series of events which causes enhanced iNOS, VEGF, PIGF, and free radicals expression.…”
Section: Resultsmentioning
confidence: 99%
“…The activity of eNOS is impaired in T2DM, 17 cardiovascular diseases, and hypertension, 15 while a disequilibrium in eNOS production is also implicated in DR onset. 13,[22][23][24] The eNOS gene is located on chromosome 7q35-36, is composed of 26 exons, and spans 21 kb. 25 The eNOS gene has numerous reported polymorphisms, which may affect NO bioavailability, exerting thus neutral, detrimental or protective effects in acute or chronic vascular diseases.…”
Section: Introductionmentioning
confidence: 99%