ReviewCurrent hypertension reports2006
The link between Glut-1 and hypertension in diabetic nephropathy.
Review in Current hypertension reports, 2006. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 3 papers.
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
3 citing papers in PubMed, 5 citations in OpenAlex.
- GLUT1 and prorenin receptor mediate differential regulation of TGF-β and CTGF in renal inner medullary collecting duct cells during high glucose conditions.Biological research · 2024Article
- Interaction mechanism between luteoloside and corn silk glycans and the synergistic role in hypoglycemic activity.Natural products and bioprospecting · 2024Article
- Comprehensive strategy for identifying extracellular vesicle surface proteins as biomarkers for chronic kidney disease.Frontiers in physiology · 2024Review
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 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Nephropathy is a major diabetic microvascular complication; both metabolic and hemodynamic perturbations play critical roles in its occurrence and progression toward end-stage renal disease. Improvements in metabolic and blood pressure control have been shown to confer protection from this diabetic complication. In this article, we review the facilitative glucose transporter Glut-1, its regulation, and its potential role in linking metabolic and hemodynamic perturbations in the pathophysiologic processes that lead to kidney injury in diabetes. We propose that an auto-maintaining mechanism of hemodynamic perturbations and increased tissue angiotensin II may be involved in the initiation and maintenance of a loop in which transforming growth factor beta1 and Glut-1 upregulation play important roles in the pathophysiology of diabetic-induced kidney lesions. The understanding of the molecular mechanisms that link glomerular hypertension and excessive glucose metabolism may provide insight into new therapeutic strategies for the treatment of diabetic renal disease.
Indexed as
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What Socratic 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 Socratic graph.