Evidence map›Paper›PMID 27231427›Full record

ArticleThe International journal of angiology : official publication of the International College of Angiology, Inc2016

Atherosclerosis and the Hypercholesterolemic AGE-RAGE Axis.

Erick McNair, Mabood Qureshi, Kailash Prasad, Colin Pearce

Open access · bronzeAbstract read
In one paragraph

Article in The International journal of angiology : official publication of the International College of Angiology, Inc, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 28 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
28citing papers in PubMed, 1 pooled it
1.9field-weighted citation impact, top 17% 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

28 citing papers in PubMed, 1 synthesis or guideline pooled it, 43 citations in OpenAlex.

  1. Pooled it
  2. Trial
  3. Article
  4. Article
  5. Review
  6. Review
  7. Article
  8. Review
  9. Review
  10. Review
  11. Article
  12. Article
  13. Concentrations of NBiomolecules · 2022
    Article
  14. Review
  15. Mechanism of Hypercholesterolemia-Induced Atherosclerosis.Reviews in cardiovascular medicine · 2022
    Review
  16. Article
  17. Article
  18. Current Status of Primary, Secondary, and Tertiary Prevention of Coronary Artery Disease.The International journal of angiology : official publication of the International College of Angiology, Inc · 2021
    Review
  19. Advanced Glycation End Products: New Clinical and Molecular Perspectives.International journal of environmental research and public health · 2021
    Review
  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

4 authors at 1 institution in 1 country.

Erick McNairDepartment of Pathology and Laboratory Medicine, University of Saskatchewan, Saskatoon, Saskatchewan, Canada.
Mabood QureshiDepartment of Pathology and Laboratory Medicine, University of Saskatchewan, Saskatoon, Saskatchewan, Canada.
Kailash PrasadDepartment of Physiology, University of Saskatchewan, Saskatoon, Saskatchewan, Canada.
Colin PearceDepartment of Medicine, University of Saskatchewan, Saskatoon, Saskatchewan, Canada.
University of Saskatchewan · CA

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Background Interaction of advanced glycation end products (AGE) with the receptor for advanced glycation end products (RAGE) has been implicated in the pathogenesis of atherosclerosis. Soluble receptors for advanced glycation end products (sRAGE) act as a decoy for AGE by competing with RAGE and suppressing developing atherosclerosis. Hypercholesterolemia and the oxidative stress are known factors involved in atherosclerosis. High-density lipoprotein cholesterol (HDL-C) is known to exert a protective effect against the development of atherosclerosis. We hypothesize that hypercholesterolemia-induced atherosclerosis may be mediated through the AGE-RAGE axis. Objectives Two objectives to be determined are: (1) if hypercholesterolemia is positively correlated with serum AGE, AGE/sRAGE, and malondialdehyde (MDA: a marker for oxidative stress) and (2) if the protective effect of HDL-C is positively associated with serum sRAGE and negatively correlated with the levels of AGE and AGE/sRAGE. Methods Measurement of serum lipid levels from 100 patients allowed the separation into two groups (hypercholesterolemic and normocholesterolemic). Measurements of serum levels of AGE, sRAGE, and MDA were performed. Results Serum levels of sRAGE were lower, while the levels of AGE and AGE/sRAGE were higher in hypercholesterolemic subjects as compared with normocholesterolemic subjects. sRAGE levels are positively correlated with HDL, while they are negatively correlated with low-density lipoprotein, triglycerides, total cholesterol, and MDA in hypercholesterolemic subjects. Conclusions Hypercholesterolemia is positively correlated with serum AGE, AGE/sRAGE, and MDA. The effect of HDL-C may be due to increases in sRAGE and decreases in the levels of AGE and AGE/sRAGE. Hypercholesterolemia-induced atherosclerosis may be mediated through the AGE-RAGE axis; however, more research must be conducted.

Indexed as

advanced glycation end productatherosclerosiscoronary arteryhypercholesterolemiaoxidative stress

Identifiers

PMID27231427
PMCPMC4870054
OpenAlexW2291888834

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.