Evidence map›Paper›PMID 30459752›Full record

ReviewFrontiers in immunology2018

The Development of Serum Amyloid P as a Possible Therapeutic.

Darrell Pilling, Richard H Gomer

Open access · goldAbstract readReview
In one paragraph

Review in Frontiers in immunology, 2018. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 61 papers.

0numbers the graph read from it
0cells of the map it votes in
61citing papers in PubMed
3.1field-weighted citation impact, top 8% 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

61 citing papers in PubMed, 87 citations in OpenAlex.

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  18. Exploring Intrinsic Disorder in Human Synucleins and Associated Proteins.International journal of molecular sciences · 2024
    Article
  19. TGF-β signaling: critical nexus of fibrogenesis and cancer.Journal of translational medicine · 2024
    Review
  20. Article

1 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.

Darrell PillingDepartment of Biology, Texas A&M University, College Station, TX, United States.
Richard H GomerDepartment of Biology, Texas A&M University, College Station, TX, United States.
Texas A&M University · US

Funding

Breaking a novel feedback loop to inhibit fibrosisR01HL132919 · NHLBI · TEXAS A&M UNIVERSITY · PI GOMER, RICHARD H · 2018 to 2021
$1.4M
Pentraxin regulation of macrophage differentiationR01HL118507 · NHLBI · TEXAS A&M UNIVERSITY · PI GOMER, RICHARD H · 2014 to 2017
$1.4M
NHLBI NIH HHS R01 HL118507NHLBI NIH HHS R01 HL132919
6 · The paper itself

Abstract

Pentraxins such as serum amyloid P (SAP; also known as PTX2) regulate several aspects of the innate immune system. SAP inhibits the differentiation of monocyte-derived fibroblast-like cells called fibrocytes, promotes the formation of immuno-regulatory macrophages, and inhibits neutrophil adhesion to extracellular matrix proteins. In this minireview, we describe how these effects of SAP have led to its possible use as a therapeutic, and how modulating SAP effects might be used for other therapeutics. Fibrosing diseases such as pulmonary fibrosis, cardiac fibrosis, liver fibrosis, and renal fibrosis are associated with 30-45% of deaths in the US. Fibrosis involves both fibrocyte differentiation and profibrotic macrophage differentiation, and possibly because SAP inhibits both of these processes, in 9 different animal models, SAP inhibited fibrosis. In Phase 1B and Phase 2 clinical trials, SAP injections reduced the decline in lung function in pulmonary fibrosis patients, and in a small Phase 2 trial SAP injections reduced fibrosis in myelofibrosis patients. Acute respiratory distress syndrome/ acute lung injury (ARDS/ALI) involves the accumulation of neutrophils in the lungs, and possibly because SAP inhibits neutrophil adhesion, SAP injections reduced the severity of ARDS in an animal model. Conversely, depleting SAP is a potential therapeutic for amyloidosis, topically removing SAP from wound fluid speeds wound healing in animal models, and blocking SAP binding to one of its receptors makes cultured macrophages more aggressive toward tuberculosis bacteria. These results suggest that modulating pentraxin signaling might be useful for a variety of diseases.

Indexed as

AmyloidosisAnimalsClinical Trials as TopicFibroblastsFibrosisHumansImmunomodulationMacrophagesMultigene FamilyNeutrophilsSerum Amyloid P-ComponentSignal TransductionTuberculosisWound HealingSerum Amyloid P-Componentfibrocytefibrosismacrophagepentraxinpulmonary fbrosisserum amyloid P component (SAP)

Identifiers

PMID30459752
PMCPMC6232687
OpenAlexW2896540448

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.