Evidence map›Paper›PMID 31135596›Full record

ReviewCurrent opinion in lipidology2019

Role of serum amyloid A in atherosclerosis.

Preetha Shridas, Lisa R Tannock

Open access · greenAbstract readReview
In one paragraph

Review in Current opinion in lipidology, 2019. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 43 papers, 2 of them syntheses that pooled it.

0numbers the graph read from it
0cells of the map it votes in
43citing papers in PubMed, 2 pooled it
2.1field-weighted citation impact, top 13% 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

43 citing papers in PubMed, 2 syntheses or guidelines pooled it, 90 citations in OpenAlex.

  1. Pooled it
  2. Pooled it
  3. Trial
  4. Article
  5. Review
  6. Article
  7. Article
  8. Serum amyloid A in HFpEF and cardiometabolic diseases.Basic research in cardiology · 2026
    Review
  9. Article
  10. Review
  11. Article
  12. Article
  13. Article
  14. Exposure ofEnvironmental health perspectives · 2024
    Article
  15. Article
  16. Osteocytes/Osteoblasts Produce SAA3 to Regulate Hepatic Metabolism of Cholesterol.Advanced science (Weinheim, Baden-Wurttemberg, Germany) · 2024
    Article
  17. Article
  18. Article
  19. 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

2 authors at 2 institutions in 2 countries.

Preetha ShridasDepartment of Internal Medicine.
Lisa R TannockDepartment of Internal Medicine.
Cardiovascular Research Center · BRUniversity of Kentucky · US

Funding

The role of IKKß in linking obesity to adipose tissue inflammation and adipogeneP20GM103527 · NIGMS · UNIVERSITY OF KENTUCKY · PI MORRIS, ANDREW J · 2012 to 2017
$13.7M
Pilot Projects ProgramP30GM127211 · NIGMS · UNIVERSITY OF KENTUCKY · PI CASSIS, LISA A · 2018 to 2022
$5.7M
Serum Amyloid A, Inflammasome Activation, and Abdominal Aortic AneurysmsR01HL134731 · NHLBI · UNIVERSITY OF KENTUCKY · PI DE BEER, FREDERICK C., WEBB, NANCY R · 2017 to 2020
$2.1M
Mechanisms regulating the atherogenic activities of serum amyloid AR01HL147381 · NHLBI · UNIVERSITY OF KENTUCKY · PI SHRIDAS, PREETHA · 2020 to 2023
$2.0M
BLRD VA I01 BX004275NHLBI NIH HHS R01 HL134731NHLBI NIH HHS R01 HL147381NIGMS NIH HHS P20 GM103527NIGMS NIH HHS P30 GM127211
6 · The paper itself

Abstract

purpose of reviewAcute phase serum amyloid A (SAA) is persistently elevated in chronic inflammatory conditions, and elevated levels predict cardiovascular risk in humans. More recently, murine studies have demonstrated that over-expression of SAA increases and deficiency/suppression of SAA attenuates atherosclerosis. Thus, beyond being a biomarker, SAA appears to play a causal role in atherogenesis. The purpose of this review is to summarize the data supporting SAA as a key player in atherosclerosis development. RECENT

findingsA number of pro-inflammatory and pro-atherogenic activities have been ascribed to SAA. However, the literature is conflicted, as recombinant SAA, and/or lipid-free SAA, used in many of the earlier studies, do not reflect the activity of native human or murine SAA, which exists largely lipid-associated. Recent literatures demonstrate that SAA activates the NLRP3 inflammasome, alters vascular function, affects HDL function, and increases thrombosis. Importantly, SAA activity appears to be regulated by its lipid association, and HDL may serve to sequester and limit SAA activity. SUMMARY: SAA has many pro-inflammatory and pro-atherogenic activities, is clearly demonstrated to affect atherosclerosis development, and may be a candidate target for clinical trials in cardiovascular diseases.

Indexed as

AnimalsAtherosclerosisBlood VesselsHumansLipoproteinsSerum Amyloid A ProteinThrombosisLipoproteinsSerum Amyloid A Protein

Identifiers

PMID31135596
PMCPMC7249237
OpenAlexW2946265121

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.