Evidence map›Paper›PMID 26515415›Full record

ReviewArteriosclerosis, thrombosis, and vascular biology2015

S100A12 and the S100/Calgranulins: Emerging Biomarkers for Atherosclerosis and Possibly Therapeutic Targets.

Adam Oesterle, Marion A Hofmann Bowman

Open access · greenAbstract readReview
In one paragraph

Review in Arteriosclerosis, thrombosis, and vascular biology, 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 77 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
77citing papers in PubMed, 1 pooled it
3.9field-weighted citation impact, top 6% 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

77 citing papers in PubMed, 1 synthesis or guideline pooled it, 108 citations in OpenAlex.

  1. Pooled it
  2. Trial
  3. Trial
  4. Review
  5. Article
  6. Article
  7. Review
  8. Article
  9. Association of Copper with Atherosclerosis and Treatment Strategies.Journal of cardiovascular translational research · 2025
    Review
  10. Modulation of Aging Diseases via RAGE Targets: A Dietary Intervention Review.Advanced science (Weinheim, Baden-Wurttemberg, Germany) · 2025
    Review
  11. Article
  12. Article
  13. Circulating protein biomarkers and their association with vulnerable plaque characteristics - a PROSPECT II substudy.International journal of cardiology. Cardiovascular risk and prevention · 2025
    Article
  14. Review
  15. Article
  16. Article
  17. Article
  18. Review
  19. Article
  20. Review

17 more citing papers are in PubMed but not listed here.

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

2 authors at 1 institution in 1 country.

Adam OesterleFrom the Department of Medicine, The University of Chicago, IL.
Marion A Hofmann BowmanFrom the Department of Medicine, The University of Chicago, IL. mhofmann@medicine.bsd.uchicago.edu.
University of Chicago · US

Funding

Re-Engineering Translational Research at the University of ChicagoUL1TR000430 · NCATS · UNIVERSITY OF CHICAGO · PI SOLWAY, JULIAN · 2012 to 2016
$20.2M
Pro-inflammatory S100 protein as disease modifier in calcific aortic valve diseasR01HL114821 · NHLBI · UNIVERSITY OF CHICAGO · PI HOFMANN BOWMAN, MARION A · 2012 to 2015
$1.5M
NCATS NIH HHS UL1 TR000430NHLBI NIH HHS R01 HL114821NHLBI NIH HHS R01HL114821
6 · The paper itself

Abstract

Atherosclerosis is mediated by local and systematic inflammation. The multiligand receptor for advanced glycation end products (RAGE) has been studied in animals and humans and is an important mediator of inflammation and atherosclerosis. This review focuses on S100/calgranulin proteins (S100A8, S100A9, and S100A12) and their receptor RAGE in mediating vascular inflammation. Mice lack the gene for S100A12, which in humans is located on chromosome 3 between S100A8 and S100A9. Transgenic mice with smooth muscle cell-targeted expression of S100A12 demonstrate increased coronary and aortic calcification, as well as increased plaque vulnerability. Serum S100A12 has recently been shown to predict future cardiovascular events in a longitudinal population study, underscoring a role for S100A12 as a potential biomarker for coronary artery disease. Genetic ablation of S100A9 or RAGE in atherosclerosis-susceptible apolipoprotein E null mice results in reduced atherosclerosis. Importantly, S100A12 and the RAGE axis can be modified pharmacologically. For example, soluble RAGE reduces murine atherosclerosis and vascular inflammation. Additionally, a class of compounds currently in phase III clinical trials for multiple sclerosis and rheumatologic conditions, the quinoline-3-carboxamides, reduce atherosclerotic plaque burden and complexity in transgenic S100A12 apolipoprotein E null mice, but have not been tested with regards to human atherosclerosis. The RAGE axis is an important mediator for inflammation-induced atherosclerosis, and S100A12 has emerged as biomarker for human atherosclerosis. Decreasing inflammation by inhibiting S100/calgranulin-mediated activation of RAGE attenuates murine atherosclerosis, and future studies in patients with coronary artery disease are warranted to confirm S100/RAGE as therapeutic target for atherosclerosis.

Indexed as

AnimalsAnti-Inflammatory AgentsAtherosclerosisBiomarkersCalgranulin ACalgranulin BDisease Models, AnimalHumansInflammationInflammation MediatorsMice, KnockoutMolecular Targeted TherapyPredictive Value of TestsPrognosisReceptor for Advanced Glycation End ProductsS100A12 ProteinAGER protein, humanAnti-Inflammatory AgentsBiomarkersCalgranulin ACalgranulin BInflammation MediatorsReceptor for Advanced Glycation End ProductsS100A12 ProteinS100A12 protein, humanapolipoprotein Eatherosclerosiscoronary artery diseaseinflammationS100A12S100/calgranulins

Identifiers

PMID26515415
PMCPMC4771489
OpenAlexW2564504700

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.