ArticleScience signaling2014
Inhibiting the response to VEGF in diabetes.
Article in Science signaling, 2014. The graph could read no effect estimate from its abstract, so it casts no vote on the map. An erratum has been issued. Cited by 8 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
8 citing papers in PubMed, 18 citations in OpenAlex.
- Multi-omics atlas of ovarian cellular and molecular responses to diabetes.Molecular metabolism · 2026Article
- Effect of Platelet-Derived Growth Factor C on Mitochondrial Oxidative Stress Induced by High d-Glucose in Human Aortic Endothelial Cells.Pharmaceuticals (Basel, Switzerland) · 2022Article
- Mechanisms of Rhizoma Coptidis against type 2 diabetes mellitus explored by network pharmacology combined with molecular docking and experimental validation.Scientific reports · 2021Article
- Systemic elucidation on the potential bioactive compounds and hypoglycemic mechanism of Polygonum multiflorum based on network pharmacology.Chinese medicine · 2020Article
- Influence of type 2 diabetes on local production of inflammatory molecules in adults with and without chronic periodontitis: a cross-sectional study.BMC oral health · 2015Article
- Inhibition of protein kinase C enhances angiogenesis induced by platelet-derived growth factor C in hyperglycemic endothelial cells.Cardiovascular diabetology · 2015Article
- High glucose induces human endothelial dysfunction through an Axl-dependent mechanism.Cardiovascular diabetology · 2014Article
- Influence of Egr-1 in cardiac tissue-derived mesenchymal stem cells in response to glucose variations.BioMed research international · 2014Article
Corrections and comments
- Comment on
- Erratum issued
Authors and funding
2 authors at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Inhibition of the vascular endothelial growth factor (VEGF)-VEGF receptor 2 (VEGFR2) signaling axis may play a role in endothelial dysfunction and serious vascular complications associated with diabetes. In this issue, Warren et al. identified a ligand-independent, receptor tyrosine kinase-independent VEGFR2 signaling pathway that is responsible for impaired responses to VEGF in diabetic endothelial cells. Reactive oxygen species (ROS) resulting from the hyperglycemic status promoted activation and subsequent degradation of VEGFR2 in a ligand-independent manner. Consequently, VEGF-VEGFR2 signaling was inhibited due to depletion of VEGFR2 at the cell surface. Activation of this ligand-independent, ROS-induced VEGFR2 signaling was mediated by the Src family of kinases and occurred in the Golgi compartment in the endothelial cells. Blocking ROS production by antioxidants effectively reversed VEGFR2 deficiency at the cell surface in hyperglycemia. These findings suggest that ROS-induced VEGFR2 signaling might be a promising new target for the treatment of vascular diseases 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.