Evidence map›Paper›PMID 15090261›Full record

ReviewJournal of cellular and molecular medicine

Anti-atherosclerotic effects of vitamin E--myth or reality?

Adelina Munteanu, J-M Zingg, A Azzi

Open access · bronzeAbstract readReview
In one paragraph

Review in Journal of cellular and molecular medicine. 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
5.8field-weighted citation impact, top 2% 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, 147 citations in OpenAlex.

  1. Trial
  2. Article
  3. Article
  4. Oxidized LDLs as Signaling Molecules.Antioxidants (Basel, Switzerland) · 2021
    Review
  5. Article
  6. Saudi journal of biological sciences · 2018
    Article
  7. Review
  8. Article
  9. Article
  10. Article
  11. Article
  12. Article
  13. Article
  14. Review
  15. Isoforms of Vitamin E Differentially Regulate PKCJournal of clinical & cellular immunology · 2013
    Article
  16. Review
  17. Review
  18. Isoforms of vitamin E differentially regulate inflammation.Endocrine, metabolic & immune disorders drug targets · 2010
    Review
  19. Article
  20. Review
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

3 authors at 1 institution in 1 country.

Adelina MunteanuInstitute of Biochemistry and Molecular Biology, University of Bern, Bern, Switzerland.
J-M Zingg
A Azzi
University of Bern · CH

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Atherosclerosis and its complications such as coronary heart disease, myocardial infarction and stroke are the leading causes of death in the developed world. High blood pressure, diabetes, smoking and a diet high in cholesterol and lipids clearly increase the likelihood of premature atherosclerosis, albeit other factors, such as the individual genetic makeup, may play an additional role. Several epidemiological studies and intervention trials have been performed with vitamin E, and some of them showed that it prevents atherosclerosis. For a long time, vitamin E was assumed to act by decreasing the oxidation of LDL, a key step in atherosclerosis initiation. However, at the cellular level, vitamin E acts by inhibition of smooth muscle cell proliferation, platelet aggregation, monocyte adhesion, oxLDL uptake and cytokine production, all reactions implied in the progression of atherosclerosis. Recent research revealed that these effects are not the result of the antioxidant activity of vitamin E, but rather of precise molecular actions of this compound. It is assumed that specific interactions of vitamin E with enzymes and proteins are at the basis of its non-antioxidant effects. Vitamin E influences the activity of several enzymes (e.g. PKC, PP2A, COX-2, 5-lipooxygenase, nitric oxide synthase, NADPH-oxidase, superoxide dismutase, phopholipase A2) and modulates the expression of genes that are involved in atherosclerosis (e.g. scavenger receptors, integrins, selectins, cytokines, cyclins). These interactions promise to reveal the biological properties of vitamin E and allow designing better strategies for the protection against atherosclerosis progression.

Indexed as

AdultAgedalpha-TocopherolAnimalsAntioxidantsApoptosisArteriosclerosisBiological TransportCell AdhesionClinical Trials as TopicCyclooxygenase 2Cyclooxygenase 2 InhibitorsCyclooxygenase InhibitorsDisease Models, AnimalFemaleHumansalpha-TocopherolAntioxidantsCyclooxygenase 2Cyclooxygenase 2 InhibitorsCyclooxygenase InhibitorsIsoenzymesLipoxygenase InhibitorsMembrane ProteinsNitric Oxide SynthasePhosphoprotein PhosphatasesProstaglandin-Endoperoxide SynthasesProtein Kinase CPTGS2 protein, humanSuperoxide DismutaseVitamin E

Identifiers

PMID15090261
PMCPMC6740318
OpenAlexW2037726433

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.