ArticleJournal of cell science2005
Oxidative stress inactivates VEGF survival signaling in retinal endothelial cells via PI 3-kinase tyrosine nitration.
Article in Journal of cell science, 2005. The graph could read no effect estimate from its abstract, so it casts no vote on the map. It has been retracted, and should not be counted. Cited by 65 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
65 citing papers in PubMed, 149 citations in OpenAlex.
- Phytoestrogen α-Zearalanol attenuates homocysteine-induced apoptosis in human umbilical vein endothelial cells.BioMed research international · 2013Trial
- Network pharmacology mechanism of Scutellarin to inhibit RGC pyroptosis in diabetic retinopathy.Scientific reports · 2023Article
- Review
- Bradykinin Type 1 Receptor - Inducible Nitric Oxide Synthase: A New Axis Implicated in Diabetic Retinopathy.Frontiers in pharmacology · 2019Article
- Models of retinal diseases and their applicability in drug discovery.Expert opinion on drug discovery · 2018Review
- Acute and Chronic Hyperglycemia Elicit JIP1/JNK-Mediated Endothelial Vasodilator Dysfunction of Retinal Arterioles.Investigative ophthalmology & visual science · 2016Article
- Neuroprotection as a Therapeutic Target for Diabetic Retinopathy.Journal of diabetes research · 2016Review
- Protective effects of Phyllanthus emblica against myocardial ischemia-reperfusion injury: the role of PI3-kinase/glycogen synthase kinase 3β/β-catenin pathway.Journal of physiology and biochemistry · 2015Article
- Metformin treatment in the period after stroke prevents nitrative stress and restores angiogenic signaling in the brain in diabetes.Diabetes · 2015Article
- Silencing p75(NTR) prevents proNGF-induced endothelial cell death and development of acellular capillaries in rat retina.Molecular therapy. Methods & clinical development · 2015Article
- Primary retinal cultures as a tool for modeling diabetic retinopathy: an overview.BioMed research international · 2015Review
- Hyperthermia-induced upregulation of vascular endothelial growth factor in retinal pigment epithelial cells is regulated by mitogen-activated protein kinases.Graefe's archive for clinical and experimental ophthalmology = Albrecht von Graefes Archiv fur klinische und experimentelle Ophthalmologie · 2014Article
- Candesartan induces a prolonged proangiogenic effect and augments endothelium-mediated neuroprotection after oxygen and glucose deprivation: role of vascular endothelial growth factors A and B.The Journal of pharmacology and experimental therapeutics · 2014Article
- Diabetic retinopathy: loss of neuroretinal adaptation to the diabetic metabolic environment.Annals of the New York Academy of Sciences · 2014Review
- Cerebral neovascularization in diabetes: implications for stroke recovery and beyond.Journal of cerebral blood flow and metabolism : official journal of the International Society of Cerebral Blood Flow and Metabolism · 2014Review
- Article
- Lycopene ameliorates renal function in rats with streptozotocin-induced diabetes.International journal of clinical and experimental pathology · 2014Article
- Transforming growth factor-β regulates endothelial function during high salt intake in rats.Hypertension (Dallas, Tex. : 1979) · 2013Article
- Hyperactivation of retina by light in mice leads to photoreceptor cell death mediated by VEGF and retinal pigment epithelium permeability.Cell death & disease · 2013Article
- Antioxidants and diabetic retinopathy.Current diabetes reports · 2013Review
5 more citing papers are in PubMed but not listed here.
Corrections and comments
- Expression of concern · 2017-05-15Duplication of/in Image · Falsification/Fabrication of Image · Investigation by Company/Institution · Investigation by Journal/Publisher · Investigation by Third Party · Legal Reasons and/or Threats · Manipulation of Images · Misconduct - Official Investigation(s) and/or Finding(s) · Misconduct by Author · Objections by Author(s) · Objections by Third Party · Unreliable Results and/or Conclusions · Upgrade/Update of Prior Notice(s) · · AB El-Remessy named for misconduct; this notice adds further information to the prior retraction notice
- Retraction · 2016-08-15Duplication of/in Image · Falsification/Fabrication of Image · Investigation by Company/Institution · Investigation by Journal/Publisher · Investigation by Third Party · Manipulation of Images · Misconduct - Official Investigation(s) and/or Finding(s) · Misconduct by Author · Unreliable Results and/or Conclusions · · AB El-Remessy named for misconduct; This retraction has an update/Publisher's Note;
- Commented on by
- Retracted
Authors and funding
5 authors at 1 institution in 1 country.
Funding
Abstract
In diabetic retinopathy, endothelial cell apoptosis is paradoxically increased despite upregulation of the potent pro-survival factor VEGF. We tested the hypothesis that elevated glucose levels disrupt VEGF's pro-survival function via peroxynitrite-mediated alteration of the Akt-1/p38 MAP kinase signaling pathway by studies of retinal endothelial cells in vitro. High glucose or exogenous peroxynitrite caused significant increases in apoptosis in the presence or absence of VEGF. Treatment with a peroxynitrite decomposition catalyst blocked these effects, implying a causal role of peroxynitrite. Peroxynitrite or high glucose treatment also increased phosphorylation of p38 MAP kinase, whereas phosphorylation of Akt-1 was significantly decreased in basal or VEGF-stimulated conditions. High glucose- or peroxynitrite-treated cells also showed significant increases in tyrosine nitration on the p85 subunit of PI 3-kinase that blocked PI 3-kinase and Akt-1 kinase activity. Inhibiting peroxynitrite formation or blocking tyrosine nitration of p85 restored the activity of PI 3-kinase and Akt-1 kinase, blocked phosphorylation of p38 MAP kinase and normalized pro-survival function. Transfecting the cells with constitutively active Akt-1 or inhibiting activity of p38 MAP kinase completely masked the pro-apoptotic effects of high glucose and exogenous peroxynitrite, suggesting an interaction between the Akt-1 and p38 MAP kinase pathways. In conclusion, high glucose treatment blocks the pro-survival effect of VEGF and causes accelerated endothelial cell apoptosis via the action of peroxynitrite in causing tyrosine nitration of PI 3-kinase, inhibiting activity of Akt-1 kinase and increasing the activity of p38 MAP kinase.
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.