Evidence map›Paper›PMID 22572850›Full record

ArticleAmerican journal of physiology. Cell physiology2012

Rosiglitazone attenuates NF-κB-mediated Nox4 upregulation in hyperglycemia-activated endothelial cells.

Clintoria R Williams, Xianghuai Lu, Roy L Sutliff, C Michael Hart

Open access · greenAbstract read
In one paragraph

Article in American journal of physiology. Cell physiology, 2012. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 30 papers.

0numbers the graph read from it
0cells of the map it votes in
30citing 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

30 citing papers in PubMed, 61 citations in OpenAlex.

  1. Article
  2. Review
  3. Review
  4. Hepatoprotective Effect ofOxidative medicine and cellular longevity · 2022
    Article
  5. Article
  6. PPAR-PPAR research · 2022
    Article
  7. Article
  8. Article
  9. Article
  10. Article
  11. SIRT1-NOX4 signaling axis regulates cancer cachexia.The Journal of experimental medicine · 2020
    Article
  12. Article
  13. Article
  14. Review
  15. Review
  16. Article
  17. Autologous fat transplants to deliver glitazone and adiponectin for vasculoprotection.Journal of controlled release : official journal of the Controlled Release Society · 2017
    Article
  18. Article
  19. Hypoxia inhibits expression and function of mitochondrial thioredoxin 2 to promote pulmonary hypertension.American journal of physiology. Lung cellular and molecular physiology · 2017
    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

4 authors at 1 institution in 1 country.

Clintoria R WilliamsDepartment of Medicine, Atlanta Veterans Affairs and Emory University Medical Centers, Georgia, USA.
Xianghuai Lu
Roy L Sutliff
C Michael Hart
Emory University · US

Funding

PPAR gamma regulates vascular endothelial reactive species production in diabetesR01DK074518 · NIDDK · EMORY UNIVERSITY · PI HART, C MICHAEL · 2008 to 2012
$1.6M
NIDDK NIH HHS R01DK074518
6 · The paper itself

Abstract

Vascular complications, a major cause of morbidity and mortality in diabetic patients, are related to hyperglycemia-induced oxidative stress. Previously, we reported that rosiglitazone (RSG) attenuated vascular expression and activity of NADPH oxidases in diabetic mice. The mechanisms underlying these effects remain to be elucidated. We hypothesized that RSG acts directly on endothelial cells to modulate vascular responses in diabetes. To test this hypothesis, human aortic endothelial cells (HAECs) were exposed to normal glucose (NG; 5.6 mmol/l) or high glucose (HG; 30 mmol/l) concentrations. Select HAEC monolayers were treated with RSG, caffeic acid phenethyl ester (CAPE), diphenyleneiodonium (DPI), small interfering (si)RNA (to NF-κB/p65 or Nox4), or Tempol. HG increased the expression and activity of the NADPH oxidase catalytic subunit Nox4 but not Nox1 or Nox2. RSG attenuated HG-induced NF-κB/p65 phosphorylation, nuclear translocation, and binding to the Nox4 promoter. Inhibiting NF-κB with CAPE or siNF-κB/p65 also reduced HG-induced Nox4 expression and activity. HG-induced H(2)O(2) production was attenuated by siRNA-mediated knockdown of Nox4, and HG-induced HAEC monocyte adhesion was attenuated by treatment with RSG, DPI, CAPE, or Tempol. These results indicate that HG exposure stimulates HAEC NF-κB activation, Nox4 expression, and H(2)O(2) production and that RSG attenuates HG-induced oxidative stress and subsequent monocyte-endothelial interactions by attenuating NF-κB/p65 activation and Nox4 expression. This study provides novel insights into mechanisms by which the thiazolidinedione peroxisome proliferator-activated receptor-γ ligand RSG favorably modulates endothelial responses in the diabetic vasculature.

Indexed as

Cells, CulturedEndothelial CellsHumansHyperglycemiaNADPH Oxidase 4NADPH OxidasesNF-kappa BOxidative StressRosiglitazoneThiazolidinedionesUp-RegulationVasodilator AgentsNADPH Oxidase 4NADPH OxidasesNF-kappa BNOX4 protein, humanRosiglitazoneThiazolidinedionesVasodilator Agents

Identifiers

PMID22572850
PMCPMC3629986
OpenAlexW2123761524

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.