ArticleJournal of ocular biology, diseases, and informatics2011
Nuclear GAPDH: changing the fate of Müller cells in diabetes.
Article in Journal of ocular biology, diseases, and informatics, 2011. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 8 papers.
What it found
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Who cites it
8 citing papers in PubMed, 13 citations in OpenAlex.
- Genome-wide association study of the response of patients with diabetic macular edema to intravitreal Anti-VEGF injection.Scientific reports · 2022Article
- Single-cell transcriptome analysis of the Akimba mouse retina reveals cell-type-specific insights into the pathobiology of diabetic retinopathy.Diabetologia · 2020Article
- Glucose Response by Stem Cell-Derived β Cells In Vitro Is Inhibited by a Bottleneck in Glycolysis.Cell reports · 2020Article
- Glyceraldehyde-3-phosphate Dehydrogenase is a Multifaceted Therapeutic Target.Pharmaceutics · 2020Review
- Models of retinal diseases and their applicability in drug discovery.Expert opinion on drug discovery · 2018Review
- Dexamethasone protects retinal ganglion cells but not Müller glia against hyperglycemia in vitro.PloS one · 2018Article
- Primary retinal cultures as a tool for modeling diabetic retinopathy: an overview.BioMed research international · 2015Review
- Detection of type 2 diabetes related modules and genes based on epigenetic networks.BMC systems biology · 2014Article
Corrections and comments
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Authors and funding
2 authors at 2 institutions in 1 country.
Funding
Abstract
Müller cells, the primary glial cells are a crucial component of the retinal tissue performing a wide range of functions including maintaining the blood-retinal barrier. Several studies suggest that diabetes leads to Müller cell dysfunction and loss. The pathophysiology of hyperglycemia-induced cellular injury of Müller cells remains only poorly understood. Recently, the concept that translocation of the predominantly cytosolic glycolytic enzyme glyceraldehyde-3-phosphate dehydrogenase (GAPDH) to the nucleus and its accumulation in this cellular compartment alters transcriptional events associated with cell death induction has gained major interest. High glucose conditions induce nuclear translocation and accumulation of GAPDH in the nucleus of Müller cells in vivo and in vitro. With regards to Müller cell dysfunction, the effects of nuclear accumulation of GAPDH are multifaceted. Considering the functional versatility of GAPDH including gene regulation, DNA repair, telomere protection, etc., it is of immense importance to explore possible GAPDH actions to unravel the mysteries around the role of GAPDH in hyperglycemia-induced cellular changes in order to develop novel therapeutic strategies. Therefore, this review focuses on the molecular events associated with the nuclear translocation of GAPDH and how it affects the fate of Müller cells in diabetes.
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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.