ReviewPediatric nephrology (Berlin, Germany)2005
Glucose transporters in diabetic nephropathy.
Review in Pediatric nephrology (Berlin, Germany), 2005. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 16 papers, 1 of them a synthesis that pooled it.
What it found
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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
16 citing papers in PubMed, 1 synthesis or guideline pooled it, 55 citations in OpenAlex.
- Relationship between five GLUT1 gene single nucleotide polymorphisms and diabetic nephropathy: a systematic review and meta-analysis.Molecular biology reports · 2012Pooled it
- Human Glucose Transporters in Renal Glucose Homeostasis.International journal of molecular sciences · 2021Review
- Glucolipotoxicity: A Proposed Etiology for Wooden Breast and Related Myopathies in Commercial Broiler Chickens.Frontiers in physiology · 2020Article
- Ion channels and transporters in diabetic kidney disease.Current topics in membranes · 2019Review
- Diabetes, a Contemporary Risk for Parkinson's Disease: Epidemiological and Cellular Evidences.Frontiers in aging neuroscience · 2019Article
- Saving the sweetness: renal glucose handling in health and disease.American journal of physiology. Renal physiology · 2017Review
- Activation of general control nonderepressible 2 kinase protects human glomerular endothelial cells from harmful high-glucose-induced molecular pathways.International urology and nephrology · 2016Article
- GLUT1 enhances mTOR activity independently of TSC2 and AMPK.American journal of physiology. Renal physiology · 2011Article
- A fluorescence method for measurement of glucose transport in kidney cells.Diabetes technology & therapeutics · 2011Article
- A glimpse of various pathogenetic mechanisms of diabetic nephropathy.Annual review of pathology · 2011Review
- Altered gene expression profiles in the brain, kidney, and lung of deceased neonatal cloned pigs.Cellular reprogramming · 2010Article
- Podocyte-specific overexpression of GLUT1 surprisingly reduces mesangial matrix expansion in diabetic nephropathy in mice.American journal of physiology. Renal physiology · 2010Article
- Frequency distribution of XbaIG > T and HaeIIIT > C GLUT1 polymorphisms among different Brazilian ethnic groups.Molecular biology reports · 2010Article
- Enhanced expression of Janus kinase-signal transducer and activator of transcription pathway members in human diabetic nephropathy.Diabetes · 2009Article
- Rosiglitazone reduces renal and plasma markers of oxidative injury and reverses urinary metabolite abnormalities in the amelioration of diabetic nephropathy.American journal of physiology. Renal physiology · 2008Article
- GLUT2 protein at the rat proximal tubule brush border membrane correlates with protein kinase C (PKC)-betal and plasma glucose concentration.Diabetologia · 2007Article
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
Changes in glucose transporter expression in glomerular cells occur early in diabetes. These changes, especially the GLUT1 increase in mesangial cells, appear to play a pathogenic role in the development of ECM expansion and perhaps other features of diabetic nephropathy. In addition, it appears that at least some diabetic patients may be predisposed to nephropathy because of polymorphisms in their GLUT1 genes. GLUT1 overexpression leads to increased glucose metabolic flux which in turn triggers the polyol pathway and activation of PKC alpha and B1. Activation of these PKC isoforms can lead directly to AP-1 induced increases in fibronectin expression and ECM accumulation. Other, more novel effects of GLUT1 on cellular hypertrophy and injury could also promote changes of diabetic nephropathy. Strategies to prevent GLUT1 overexpression could ameliorate or prevent the progression of diabetic nephropathy.
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.