ArticleBiochemical and biophysical research communications2009
Translocation of H-Ras and its implications in the development of diabetic retinopathy.
Article in Biochemical and biophysical research communications, 2009. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 14 papers.
What it found
Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.
The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
The trial behind it
Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.
Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.
Who cites it
14 citing papers in PubMed, 18 citations in OpenAlex.
- Paeoniflorin alleviates high glucose-induced endothelial cell apoptosis in diabetes mellitus by inhibiting HRAS-activated RAS pathway.Endocrine journal · 2024Article
- Redox-sensitive small GTPase H-Ras in murine astrocytes, anRedox report : communications in free radical research · 2022Article
- Identification and Validation of Autophagy-Related Genes in Diabetic Retinopathy.Frontiers in endocrinology · 2022Article
- Cysteine-based regulation of redox-sensitive Ras small GTPases.Redox biology · 2019Review
- Oxidative Stress-Related Mechanisms and Antioxidant Therapy in Diabetic Retinopathy.Oxidative medicine and cellular longevity · 2017Review
- Transcription factor Nrf2-mediated antioxidant defense system in the development of diabetic retinopathy.Investigative ophthalmology & visual science · 2013Article
- Inhibition of Rho and Rac geranylgeranylation by atorvastatin is critical for preservation of endothelial junction integrity.PloS one · 2013Article
- Diabetic retinopathy and signaling mechanism for activation of matrix metalloproteinase-9.Journal of cellular physiology · 2012Article
- Role of matrix metalloproteinase-2 and -9 in the development of diabetic retinopathy.Journal of ocular biology, diseases, and informatics · 2012Article
- The role of Raf-1 kinase in diabetic retinopathy.Expert opinion on therapeutic targets · 2011Review
- Diabetic retinopathy, superoxide damage and antioxidants.Current pharmaceutical biotechnology · 2011Review
- Matrix metalloproteinase-2 in the development of diabetic retinopathy and mitochondrial dysfunction.Laboratory investigation; a journal of technical methods and pathology · 2010Article
- Role of matrix metalloproteinase-9 in the development of diabetic retinopathy and its regulation by H-Ras.Investigative ophthalmology & visual science · 2010Article
- Glyceraldehyde-3-phosphate dehydrogenase in retinal microvasculature: implications for the development and progression of diabetic retinopathy.Investigative ophthalmology & visual science · 2010Article
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
2 authors at 2 institutions in 1 country.
Funding
Abstract
H-Ras, a small molecular weight G-protein, undergoes post-translational modifications enabling its translocation from cytosol to the membrane. Hyperglycemia increases apoptosis of retinal capillary cells via activation of H-Ras, which can be ameliorated by farnesylation inhibitors. Our aim is to investigate the mechanism of retinal H-Ras activation in diabetes. H-Ras and Raf-1 were quantified in the retinal membrane and cytosol fractions obtained from streptozotocin-induced diabetes rats, and the role of post-translation modification was determined by investigating the effect of simvastatin on diabetes-induced alterations. The effect of H-Ras-siRNA on membrane translocation and apoptosis was also determined in bovine retinal endothelial cells (BRECs). Diabetes increased expressions of H-Ras and Raf-1 in the retinal membranes, and simvastatin prevented such translocation. Glucose-exposure of BRECs increased membrane H-Ras expression and H-Ras-siRNA prevented this translocation, and also decreased their apoptosis. Thus, membrane translocation of H-Ras is a plausible mechanism responsible for accelerated apoptosis of retinal capillary cells in diabetes.
Indexed as
Identifiers
What OpenQuestion holds
Registered trials
Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.