Evidence map›Paper›PMID 25429103›Full record

ArticleJournal of lipid research2015

A brief elevation of serum amyloid A is sufficient to increase atherosclerosis.

Joel C Thompson, Colton Jayne, Jennifer Thompson, Patricia G Wilson, Meghan H Yoder, Nancy Webb, Lisa R Tannock

Open access · hybridAbstract read
In one paragraph

Article in Journal of lipid research, 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 57 papers.

0numbers the graph read from it
0cells of the map it votes in
57citing papers in PubMed
7.9field-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

57 citing papers in PubMed, 87 citations in OpenAlex.

  1. Trial
  2. Article
  3. Serum amyloid A in HFpEF and cardiometabolic diseases.Basic research in cardiology · 2026
    Review
  4. Article
  5. Article
  6. Serum Amyloid A: A Double-Edged Sword in Health and Disease.International journal of molecular sciences · 2025
    Review
  7. Article
  8. Article
  9. Osteocytes/Osteoblasts Produce SAA3 to Regulate Hepatic Metabolism of Cholesterol.Advanced science (Weinheim, Baden-Wurttemberg, Germany) · 2024
    Article
  10. Review
  11. Article
  12. Review
  13. Article
  14. Article
  15. Inflammatory Mediators in Atherosclerotic Vascular Remodeling.Frontiers in cardiovascular medicine · 2022
    Review
  16. Review
  17. Article
  18. Article
  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

7 authors at 1 institution in 1 country.

Joel C ThompsonDepartment of Internal Medicine, Division of Endocrinology and Molecular Medicine, University of Kentucky, Lexington, KY Department of Pharmacology and Nutritional Sciences, Division of Nutritional Sciences, University of Kentucky, Lexington, KY.
Colton JayneDepartment of Internal Medicine, Division of Endocrinology and Molecular Medicine, University of Kentucky, Lexington, KY.
Jennifer ThompsonDepartment of Internal Medicine, Division of Endocrinology and Molecular Medicine, University of Kentucky, Lexington, KY.
Patricia G WilsonDepartment of Internal Medicine, Division of Endocrinology and Molecular Medicine, University of Kentucky, Lexington, KY.
Meghan H YoderDepartment of Internal Medicine, Division of Endocrinology and Molecular Medicine, University of Kentucky, Lexington, KY.
Nancy WebbDepartment of Pharmacology and Nutritional Sciences, Division of Nutritional Sciences, University of Kentucky, Lexington, KY Barnstable Brown Diabetes and Obesity Research Center, University of Kentucky, Lexington, KY.
Lisa R TannockDepartment of Internal Medicine, Division of Endocrinology and Molecular Medicine, University of Kentucky, Lexington, KY Barnstable Brown Diabetes and Obesity Research Center, University of Kentucky, Lexington, KY Department of Veterans Affairs, Lexington, KY.
University of Kentucky · US

Funding

The role of IKKß in linking obesity to adipose tissue inflammation and adipogeneP20GM103527 · NIGMS · UNIVERSITY OF KENTUCKY · PI CASSIS, LISA A · 2012 to 2017
$13.7M
Role of Serum Amyloid A in AtheroscierosisR01HL096589 · NHLBI · UNIVERSITY OF KENTUCKY · PI TANNOCK, LISA R · 2009 to 2010
$799k
NHLBI NIH HHS R01 HL096589NHLBI NIH HHS R01HL096589NIGMS NIH HHS 8 P20 GM103527NIGMS NIH HHS P20 GM103527PHS HHS 12PRE12060285
6 · The paper itself

Abstract

Serum amyloid A (SAA) has a number of proatherogenic effects including induction of vascular proteoglycans. Chronically elevated SAA was recently shown to increase atherosclerosis in mice. The purpose of this study was to determine whether a brief increase in SAA similarly increased atherosclerosis in a murine model. The recombination activating gene 1-deficient (rag1(-/-)) × apolipoprotein E-deficient (apoe(-/-)) and apoe(-/-) male mice were injected, multiple times or just once respectively, with an adenoviral vector encoding human SAA1 (ad-SAA); the injected mice and controls were maintained on chow for 12-16 weeks. Mice receiving multiple injections of ad-SAA, in which SAA elevation was sustained, had increased atherosclerosis compared with controls. Strikingly, mice receiving only a single injection of ad-SAA, in which SAA was only briefly elevated, also had increased atherosclerosis compared with controls. Using in vitro studies, we demonstrate that SAA treatment leads to increased LDL retention, and that prevention of transforming growth factor beta (TGF-β) signaling prevents SAA-induced increases in LDL retention and SAA-induced increases in vascular biglycan content. We propose that SAA increases atherosclerosis development via induction of TGF-β, increased vascular biglycan content, and increased LDL retention. These data suggest that even short-term inflammation with concomitant increase in SAA may increase the risk of developing CVD.

Indexed as

AnimalsApolipoproteins EAtherosclerosisCardiovascular DiseasesCells, CulturedDisease Models, AnimalHomeodomain ProteinsMaleMiceMice, KnockoutProteoglycansSerum Amyloid A ProteinTransforming Growth Factor betaApolipoproteins EHomeodomain ProteinsProteoglycansRAG-1 proteinSerum Amyloid A ProteinTransforming Growth Factor betaapolipoproteinscardiovascular diseaseextracellular matrixfree-form: biglycanlipoproteinsproteoglycanstransforming growth factor betavascular biology

Identifiers

PMID25429103
PMCPMC4306683
OpenAlexW2079948512

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.