Evidence map›Paper›PMID 29094329›Full record

ArticleInternational urology and nephrology2018

Allopurinol protects human glomerular endothelial cells from high glucose-induced reactive oxygen species generation, p53 overexpression and endothelial dysfunction.

Theodoros Eleftheriadis, Georgios Pissas, Georgia Antoniadi, Vassilios Liakopoulos, Ioannis Stefanidis

Abstract read
PubMed Publisher
In one paragraph

Article in International urology and nephrology, 2018. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 21 papers.

0numbers the graph read from it
0cells of the map it votes in
21citing papers in PubMed
2.4field-weighted citation impact, top 11% of its field
1 · What the graph read from it

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.

2 · The registry

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.

3 · Its place in the literature

Who cites it

21 citing papers in PubMed, 33 citations in OpenAlex.

  1. Trial
  2. Endothelial Metabolic Reprogramming Links Diabetes to Atherosclerosis.Diabetes, metabolic syndrome and obesity : targets and therapy · 2026
    Review
  3. Article
  4. Review
  5. Review
  6. Article
  7. Article
  8. Article
  9. Article
  10. Article
  11. Review
  12. Article
  13. Review
  14. Review
  15. Article
  16. Observational
  17. Article
  18. Review
  19. Article
  20. Article
4 · The record

Corrections and comments

PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.

5 · Who and what money

Authors and funding

5 authors at 1 institution in 1 country.

Theodoros EleftheriadisDepartment of Nephrology, Faculty of Medicine, University of Thessaly, Neo Ktirio, Mezourlo Hill, 41110, Larissa, Greece. teleftheriadis@yahoo.com.ORCID http://orcid.org/0000-0001-9302-1633
Georgios PissasDepartment of Nephrology, Faculty of Medicine, University of Thessaly, Neo Ktirio, Mezourlo Hill, 41110, Larissa, Greece.
Georgia AntoniadiDepartment of Nephrology, Faculty of Medicine, University of Thessaly, Neo Ktirio, Mezourlo Hill, 41110, Larissa, Greece.
Vassilios LiakopoulosDepartment of Nephrology, Faculty of Medicine, University of Thessaly, Neo Ktirio, Mezourlo Hill, 41110, Larissa, Greece.
Ioannis StefanidisDepartment of Nephrology, Faculty of Medicine, University of Thessaly, Neo Ktirio, Mezourlo Hill, 41110, Larissa, Greece.
University of Thessaly · GR

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

purposeMitochondrial reactive oxygen species (ROS) overproduction in capillary endothelial cells is a prerequisite for the development of diabetic nephropathy. Inhibition of xanthine oxidase, another ROS generator, ameliorates experimental diabetic nephropathy. To test the hypothesis that the initial high glucose-induced ROS production by the mitochondria activates xanthine oxidase, which afterward remains as the major source of ROS, we cultured primary human glomerular endothelial cells (GEnC) under normal or high-glucose conditions, with or without the xanthine oxidase inhibitor allopurinol.

methodsROS generation and nitric oxide synthase (NOS) activity were assessed by chemiluminescence or colorimetrically. Levels of intercellular adhesion molecule 1 (ICAM-1), p53 and phosphorylated p53 (p-p53) were assessed by western blotting.

resultsAllopurinol prevented high glucose-induced ROS generation indicating that xanthine oxidase is the major source of ROS. Allopurinol protected GEnC from endothelial dysfunction since it prevented the high glucose-induced decrease in NOS activity and increase in ICAM-1 expression. Allopurinol reduced p53 and p-p53 levels induced by high glucose suggesting an axis of xanthine oxidase-derived ROS, DNA damage, p53 stabilization and endothelial dysfunction that may contribute to the pathogenesis of diabetic nephropathy.

conclusionsAllopurinol protects GEnC from high glucose-induced ROS generation, p53 overexpression and endothelial dysfunction. These data provide a pathogenetic mechanism that supports the results of experimental and clinical studies about the beneficial effect of xanthine oxidase inhibitors on the development of diabetic nephropathy.

Indexed as

AllopurinolCells, CulturedCell SurvivalEndothelial CellsFree Radical ScavengersGlucoseHumansIntercellular Adhesion Molecule-1Kidney GlomerulusNitric Oxide SynthasePrimary Cell CultureReactive Oxygen SpeciesTumor Suppressor Protein p53AllopurinolFree Radical ScavengersGlucoseICAM1 protein, humanIntercellular Adhesion Molecule-1Nitric Oxide SynthaseReactive Oxygen SpeciesTumor Suppressor Protein p53AllopurinolDiabetic nephropathyEndothelial dysfunctionp53Reactive oxygen speciesXanthine oxidase

Identifiers

PMID29094329
OpenAlexW2766171711

What OpenQuestion holds

Textmetadata
Read underepoch 390

Registered trials

None linked

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.