Evidence map›Paper›PMID 18574454›Full record

ArticleBritish journal of pharmacology2008

Raloxifene protects endothelial cell function against oxidative stress.

C M Wong, L M Yung, F P Leung, S-Y Tsang, C L Au, Z-Y Chen, X Yao, C H K Cheng, C-W Lau, M Gollasch and 1 more

Open access · greenAbstract read
In one paragraph

Article in British journal of pharmacology, 2008. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 20 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
20citing papers in PubMed, 1 pooled it
2.1field-weighted citation impact, top 13% 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

20 citing papers in PubMed, 1 synthesis or guideline pooled it, 35 citations in OpenAlex.

  1. The mechanism of vascular calcification - a systematic review.Medical science monitor : international medical journal of experimental and clinical research · 2012
    Pooled it
  2. Trial
  3. Trial
  4. Article
  5. Review
  6. Review
  7. Review
  8. Sex differences in abdominal aortic aneurysms.American journal of physiology. Heart and circulatory physiology · 2018
    Review
  9. Article
  10. Article
  11. Article
  12. Article
  13. Article
  14. Article
  15. Estrogen and estrogen receptors in cardiovascular oxidative stress.Pflugers Archiv : European journal of physiology · 2013
    Review
  16. Article
  17. Review
  18. Article
  19. Membrane-initiated actions of estrogen on the endothelium.Molecular and cellular endocrinology · 2009
    Review
  20. Endothelium in pharmacology: 30 years on.British journal of pharmacology · 2009
    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

11 authors at 3 institutions in 3 countries.

C M WongInstitute of Vascular Medicine and Department of Physiology, Chinese University of Hong Kong, Hong Kong, China.
L M Yung
F P Leung
S-Y Tsang
C L Au
Z-Y Chen
X Yao
C H K Cheng
C-W Lau
M Gollasch
Y Huang
Chinese University of Hong Kong · CNCharité - Universitätsmedizin Berlin · DEGeorgetown University Medical Center · US

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

background and purposeMaintaining a delicate balance between the generation of nitric oxide (NO) and removal of reactive oxygen species (ROS) within the vascular wall is crucial to the physiological regulation of vascular tone. Increased production of ROS reduces the effect and/or bioavailability of NO, leading to an impaired endothelial function. This study tested the hypothesis that raloxifene, a selective oestrogen receptor modulator, can prevent endothelial dysfunction under oxidative stress. EXPERIMENTAL APPROACH: Changes in isometric tension were measured in rat aortic rings. The content of cyclic GMP in aortic tissue was determined by radioimmunoassay. Phosphorylation of endothelial NOS (eNOS) and Akt was assayed by Western blot analysis. KEY

resultsIn rings with endothelium, ACh-induced relaxations were attenuated by a ROS-generating reaction (hypoxanthine plus xanthine oxidase, HXXO). The impaired relaxations were ameliorated by acute treatment with raloxifene. HXXO suppressed the ACh-stimulated increase in cyclic GMP levels; this effect was antagonized by raloxifene. The improved endothelial function by raloxifene was abolished by ICI 182,780, and by wortmannin or LY294002. Raloxifene also protected endothelial cell function against H2O2. Raloxifene increased the phosphorylation of eNOS at Ser-1177 and Akt at Ser-473; this effect was blocked by ICI 182,780. Finally, raloxifene was not directly involved in scavenging ROS, and neither inhibited the activity of xanthine oxidase nor stimulated that of superoxide dismutase. CONCLUSION AND IMPLICATIONS: Raloxifene is effective against oxidative stress-induced endothelial dysfunction in vitro through an ICI 182,780-sensitive mechanism that involves the increased phosphorylation and activity of Akt and eNOS in rat aortae.

Indexed as

AnimalsAorta, ThoracicCyclic GMPEndothelial CellsEstrogen AntagonistsIn Vitro TechniquesIsometric ContractionMaleNitric OxideNitric Oxide Synthase Type IIIOxidative StressPhosphorylationProto-Oncogene Proteins c-aktRaloxifene HydrochlorideRatsRats, Sprague-DawleyCyclic GMPEstrogen AntagonistsNitric OxideNitric Oxide Synthase Type IIIProto-Oncogene Proteins c-aktRaloxifene Hydrochloride

Identifiers

PMID18574454
PMCPMC2567878
OpenAlexW1571731262

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.