Evidence map›Paper›PMID 26130702›Full record

ReviewJournal of leukocyte biology2015

Emerging functions of serum amyloid A in inflammation.

Richard D Ye, Lei Sun

Abstract readReview
PubMed Full text at PMC Publisher
In one paragraph

Review in Journal of leukocyte biology, 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 177 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
177citing papers in PubMed, 1 pooled it
8.3field-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

177 citing papers in PubMed, 1 synthesis or guideline pooled it, 313 citations in OpenAlex.

  1. Pooled it
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  4. Increased serum amyloid A in nasal polyps is associated with systemic corticosteroid insensitivity in patients with chronic rhinosinusitis with nasal polyps: a pilot study.European archives of oto-rhino-laryngology : official journal of the European Federation of Oto-Rhino-Laryngological Societies (EUFOS) : affiliated with the German Society for Oto-Rhino-Laryngology - Head and Neck Surgery · 2018
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117 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 2 institutions in 2 countries.

Richard D Ye*School of Pharmacy, Shanghai Jiao Tong University, Shanghai, China; and Department of Pharmacology, University of Illinois at Chicago, Illinois, USA ye.richard@outlook.com.
Lei Sun*School of Pharmacy, Shanghai Jiao Tong University, Shanghai, China; and Department of Pharmacology, University of Illinois at Chicago, Illinois, USA.
Shanghai Jiao Tong University · CNUniversity of Illinois Chicago · US

Funding

Role of SAA in Inflammation and ImmunityR56AI040176 · NIAID · UNIVERSITY OF ILLINOIS AT CHICAGO · PI YE, RICHARD D · 2010 to 2010
$406k
NIAID NIH HHS R56 AI040176
6 · The paper itself

Abstract

SAA is a major acute-phase protein produced in large quantity during APR. The rise of SAA concentration in blood circulation during APR has been a clinical marker for active inflammation. In the past decade, research has been conducted to determine whether SAA plays an active role during inflammation and if so, how it influences the course of inflammation. These efforts have led to the discovery of cytokine-like activities of rhSAA, which is commercially available and widely used in most of the published studies. SAA activates multiple receptors, including the FPR2, the TLRs TLR2 and TLR4, the scavenger receptor SR-BI, and the ATP receptor P2X7. More recent studies have shown that SAA not only activates transcription factors, such as NF-κB, but also plays a role in epigenetic regulation through a MyD88-IRF4-Jmjd3 pathway. It is postulated that the activation of these pathways leads to induced expression of proinflammatory factors and a subset of proteins expressed by the M2 macrophages. These functional properties set SAA apart from well-characterized inflammatory factors, such as LPS and TNF-α, suggesting that it may play a homeostatic role during the course of inflammation. Ongoing and future studies are directed to addressing unresolved issues, including the difference between rSAA and native SAA isoforms and the exact functions of SAA in physiologic and pathologic settings.

Indexed as

Acute-Phase ReactionAdenosine TriphosphateAnimalsHumansInterferon Regulatory Factor-4Interferon Regulatory FactorsJumonji Domain-Containing Histone DemethylasesLipopolysaccharidesMyeloid Differentiation Factor 88NF-kappa BReceptors, Purinergic P2X7Scavenger Receptors, Class BSerum Amyloid A ProteinSignal TransductionToll-Like Receptor 2Toll-Like Receptor 4Adenosine TriphosphateInterferon Regulatory Factor-4Interferon Regulatory FactorsJumonji Domain-Containing Histone DemethylasesKDM6B protein, humanLipopolysaccharidesMYD88 protein, humanMyeloid Differentiation Factor 88NF-kappa BP2RX7 protein, humanReceptors, Purinergic P2X7SCARB1 protein, humanScavenger Receptors, Class BSerum Amyloid A ProteinTLR2 protein, humanTLR4 protein, humanToll-Like Receptor 2Toll-Like Receptor 4Tumor Necrosis Factor-alphaacute-phase reactantscytokinesepigenetic regulationstress response

Identifiers

PMID26130702
PMCPMC6608020
OpenAlexW2216860662

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.