ArticleInvestigative ophthalmology & visual science2010
Glyceraldehyde-3-phosphate dehydrogenase in retinal microvasculature: implications for the development and progression of diabetic retinopathy.
Article in Investigative ophthalmology & visual science, 2010. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 25 papers.
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Who cites it
25 citing papers in PubMed, 39 citations in OpenAlex.
- NAD+ modulates mitochondrial vulnerability in MERTK-associated models of retinitis pigmentosa.Nature communications · 2026Article
- Insulin resistance and cognitive decline: the metabolic mechanisms linking type 2 diabetes to Alzheimer's disease.Diabetology international · 2025Review
- Retinal Gene Expression of Selective Genes and Histological Stages of Embryonic and Post-Hatch Chickens (Genes · 2022Article
- Single-cell transcriptome analysis of the Akimba mouse retina reveals cell-type-specific insights into the pathobiology of diabetic retinopathy.Diabetologia · 2020Article
- Diabetic Retinopathy: The Role of Mitochondria in the Neural Retina and Microvascular Disease.Antioxidants (Basel, Switzerland) · 2020Review
- Diabetic Retinopathy and Laser Therapy in Rats: A Protein-Protein Interaction Network Analysis.Journal of lasers in medical sciences · 2017Article
- Nutrient-sensing mTORC1: Integration of metabolic and autophagic signals.Journal of molecular and cellular cardiology · 2016Review
- Oxidative stress and epigenetic modifications in the pathogenesis of diabetic retinopathy.Progress in retinal and eye research · 2015Review
- From pathobiology to the targeting of pericytes for the treatment of diabetic retinopathy.Current diabetes reports · 2015Review
- Roles of Pyruvate, NADH, and Mitochondrial Complex I in Redox Balance and Imbalance in β Cell Function and Dysfunction.Journal of diabetes research · 2015Review
- High-resolution crystal structures of the photoreceptor glyceraldehyde 3-phosphate dehydrogenase (GAPDH) with three and four-bound NAD molecules.Protein science : a publication of the Protein Society · 2014Article
- Posttranslational modification of mitochondrial transcription factor A in impaired mitochondria biogenesis: implications in diabetic retinopathy and metabolic memory phenomenon.Experimental eye research · 2014Article
- Pathogenesis of chronic hyperglycemia: from reductive stress to oxidative stress.Journal of diabetes research · 2014Review
- Oxidative stress: implications for the development of diabetic retinopathy and antioxidant therapeutic perspectives.Oxidative medicine and cellular longevity · 2014Review
- Characterisation of potential antidiabetic-related proteins from Pleurotus pulmonarius (Fr.) Quél. (grey oyster mushroom) by MALDI-TOF/TOF mass spectrometry.BioMed research international · 2014Article
- Impaired transport of mitochondrial transcription factor A (TFAM) and the metabolic memory phenomenon associated with the progression of diabetic retinopathy.Diabetes/metabolism research and reviews · 2013Article
- Glyceraldehyde-3-phosphate dehydrogenase interacts with proapoptotic kinase mst1 to promote cardiomyocyte apoptosis.PloS one · 2013Article
- Nuclear transport: a switch for the oxidative stress-signaling circuit?Journal of signal transduction · 2012Article
- Nuclear GAPDH: changing the fate of Müller cells in diabetes.Journal of ocular biology, diseases, and informatics · 2011Article
- Epigenetic changes in mitochondrial superoxide dismutase in the retina and the development of diabetic retinopathy.Diabetes · 2011Article
Corrections and comments
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Authors and funding
3 authors at 1 institution in 1 country.
Funding
Abstract
purposeGlyceraldehyde-3-phosphate dehydrogenase (GAPDH) has been hypothesized as a mediator in the activation of multiple pathways implicated in the pathogenesis of diabetic retinopathy. The objective of this study was to understand the mechanism by which high glucose inactivates GAPDH in retinal microvascular cells.
methodsBovine retinal endothelial cells (BRECs), transfected with GAPDH, were incubated in 20 mM glucose. The effect of the overexpression of GAPDH on its activity, apoptosis, and upstream signaling pathways, protein kinase C, and hexosamine pathways was determined. The effect of the inhibitors of nitration and ribosylation on GAPDH activity, its nuclear translocation and reversal of glucose insult was also evaluated.
resultsHigh glucose decreased GAPDH activity, expression, and nuclear translocation. Overexpression of GAPDH prevented glucose-induced inhibition of its activity, nuclear translocation, apoptosis, and activation of protein kinase C and hexosamine pathways. Inhibitors of nitration and ribosylation ameliorated glucose-induced inhibition of GAPDH, and their addition during the normal glucose exposure that followed high glucose levels had a beneficial effect on GAPDH activity and the degree of nitration and ribosylation.
conclusionsIn hyperglycemia, GAPDH in retinal microvascular cells is inhibited by its covalent modifications, and this activates multiple pathways implicated in the pathogenesis of diabetic retinopathy. The agents that can directly target modification of GAPDH have potential in inhibiting the development and in arresting the progression of diabetic retinopathy.
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