Evidence map›Paper›PMID 37396595›Full record

ReviewFrontiers in cardiovascular medicine2023

Serum amyloid A and metabolic disease: evidence for a critical role in chronic inflammatory conditions.

Laura J den Hartigh, Karolline S May, Xue-Song Zhang, Alan Chait, Martin J Blaser

Open access · goldAbstract readReview
In one paragraph

Review in Frontiers in cardiovascular medicine, 2023. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 40 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
40citing papers in PubMed, 1 pooled it
9.8field-weighted citation impact, top 1% 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

40 citing papers in PubMed, 1 synthesis or guideline pooled it, 60 citations in OpenAlex.

  1. Guideline
  2. Article
  3. Article
  4. SAA4: An Underdog Within the Serum Amyloid a Superfamily?International journal of molecular sciences · 2026
    Review
  5. Article
  6. Article
  7. Article
  8. Article
  9. Serum amyloid A in HFpEF and cardiometabolic diseases.Basic research in cardiology · 2026
    Review
  10. Article
  11. Review
  12. Review
  13. Article
  14. Article
  15. Review
  16. Review
  17. Review
  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

5 authors at 2 institutions in 1 country.

Laura J den HartighDepartment of Medicine, Division of Metabolism, Endocrinology, and Nutrition, University of Washington, Seattle, WA, United States.
Karolline S MayDepartment of Medicine, Division of Metabolism, Endocrinology, and Nutrition, University of Washington, Seattle, WA, United States.
Xue-Song ZhangCenter for Advanced Biotechnology and Medicine, Rutgers University, Piscataway, NJ, United States.
Alan ChaitDepartment of Medicine, Division of Metabolism, Endocrinology, and Nutrition, University of Washington, Seattle, WA, United States.
Martin J BlaserCenter for Advanced Biotechnology and Medicine, Rutgers University, Piscataway, NJ, United States.
University of Washington · USRutgers, The State University of New Jersey · US

Funding

Diabetes, Obesity and Metabolism Training ProgramT32DK007247 · NIDDK · UNIVERSITY OF WASHINGTON · PI GREGORY J MORTON, KRISTINA Marie UTZSCHNEIDER · 1986 to 2026
$10.0M
Nutrition, Obesity and Atherosclerosis Training ProgramT32HL007028 · NHLBI · UNIVERSITY OF WASHINGTON · PI Karin E Bornfeldt · 1985 to 2026
$6.4M
Microbial, immune, metabolic perturbations by antibiotics (MIME study)U01AI122285 · NIAID · RUTGERS BIOMEDICAL AND HEALTH SCIENCES · PI MARTIN J BLASER, Steven M Holland · 2016 to 2026
$5.2M
NHLBI NIH HHS T32 HL007028NIAID NIH HHS U01 AI122285NIDDK NIH HHS T32 DK007247
6 · The paper itself

Abstract

Serum amyloid A (SAA) subtypes 1-3 are well-described acute phase reactants that are elevated in acute inflammatory conditions such as infection, tissue injury, and trauma, while SAA4 is constitutively expressed. SAA subtypes also have been implicated as playing roles in chronic metabolic diseases including obesity, diabetes, and cardiovascular disease, and possibly in autoimmune diseases such as systemic lupus erythematosis, rheumatoid arthritis, and inflammatory bowel disease. Distinctions between the expression kinetics of SAA in acute inflammatory responses and chronic disease states suggest the potential for differentiating SAA functions. Although circulating SAA levels can rise up to 1,000-fold during an acute inflammatory event, elevations are more modest (∼5-fold) in chronic metabolic conditions. The majority of acute-phase SAA derives from the liver, while in chronic inflammatory conditions SAA also derives from adipose tissue, the intestine, and elsewhere. In this review, roles for SAA subtypes in chronic metabolic disease states are contrasted to current knowledge about acute phase SAA. Investigations show distinct differences between SAA expression and function in human and animal models of metabolic disease, as well as sexual dimorphism of SAA subtype responses.

Indexed as

adipocytes, macrophagescardiovascular diseasediabetesintestineliverobesitySAA

Identifiers

PMID37396595
PMCPMC10311072
OpenAlexW4380995142

What OpenQuestion holds

Textmetadata
LicenceCC BY
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.