Evidence map›Paper›PMID 22476914›Full record

ReviewCurrent atherosclerosis reports2012

Atherosclerosis, inflammation, genetics, and stem cells: 2012 update.

Pascal J Goldschmidt-Clermont, Chunming Dong, David M Seo, Omaida C Velazquez

Open access · greenAbstract readReview
In one paragraph

Review in Current atherosclerosis reports, 2012. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 20 papers.

0numbers the graph read from it
0cells of the map it votes in
20citing papers in PubMed
2.6field-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

20 citing papers in PubMed, 40 citations in OpenAlex.

  1. Article
  2. Article
  3. Review
  4. Article
  5. Article
  6. Article
  7. Article
  8. Review
  9. Review
  10. Article
  11. Article
  12. Review
  13. Article
  14. Article
  15. Observational
  16. Article
  17. Article
  18. Pro-inflammatory genetic markers of atherosclerosis.Current atherosclerosis reports · 2013
    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

4 authors at 2 institutions in 1 country.

Pascal J Goldschmidt-ClermontCardiology Division, Department of Medicine, Hussman Institute for Human Genomics, Leonard M. Miller School of Medicine, University of Miami, FL 33136, USA. pgoldschmidt@med.miami.edu
Chunming Dong
David M Seo
Omaida C Velazquez
University of Miami · USDr. John T. Macdonald Foundation · US

Funding

SNP discoveryP01HL073042 · NHLBI · DUKE UNIVERSITY · PI NEVINS, JOSEPH R · 2002 to 2006
$13.5M
Impact of Aging on Stem Cell Repair in AtherosclerosisR01AG023073 · NIA · UNIVERSITY OF MIAMI SCHOOL OF MEDICINE · PI GOLDSCHMIDT-CLERMONT, PASCAL J. · 2004 to 2008
$1.8M
Rac, Superoxide and Antioxidants in HypertensionR01HL071536 · NHLBI · UNIVERSITY OF MIAMI SCHOOL OF MEDICINE · PI GOLDSCHMIDT-CLERMONT, PASCAL J. · 2002 to 2005
$1.5M
NHLBI NIH HHS P01 HL073042NHLBI NIH HHS R01 HL071536NIA NIH HHS R01 AG023023NIA NIH HHS R01 AG023073
6 · The paper itself

Abstract

Atherosclerosis is a peculiar form of inflammation triggered by cholesterol-rich lipoproteins and other noxious factors such as cigarette smoke, diabetes mellitus, and hypertension. Genetics also play an important role in the disease, accounting for about 40% of the risk. Of surprise in recent years of post-human genome sequencing, atherosclerosis-relevant genes discovered by non-biased techniques (ie, genome-wide association studies), did not rehash previously suspected pathways of lipid metabolism, diabetes, or hypertension. Instead these studies highlighted genes relevant to mechanisms of inflammation and stem cell biology. Only a minority of implicated genes were linked to lipid and other cardiac risk factor genes. Although such findings do not contradict the fact that atherosclerosis is triggered and exacerbated by elevated lipids, atherosclerosis "new genes" suggest that the mechanism responsible for the development of arterial lesions is more complex than a simple response to injury, where injury is necessary, but perhaps not sufficient, for disease progression.

Indexed as

Genetic Predisposition to DiseaseAnimalsAtherosclerosisEndothelial CellsEndothelium, VascularGene Expression RegulationGenome-Wide Association StudyHumansInflammationModels, GeneticStem Cells

Identifiers

PMID22476914
PMCPMC3537163
OpenAlexW2033365282

What OpenQuestion holds

Textmetadata
LicenceTDM
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.