Evidence map›Paper›PMID 25753272›Full record

ReviewImmunology and cell biology2015

Inflammation-induced foam cell formation in chronic inflammatory disease.

Thomas A Angelovich, Anna C Hearps, Anthony Jaworowski

Open access · bronzeAbstract readReview
PubMed Publisher
In one paragraph

Review in Immunology and cell biology, 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 33 papers.

0numbers the graph read from it
0cells of the map it votes in
33citing papers in PubMed
3.0field-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

33 citing papers in PubMed, 72 citations in OpenAlex.

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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

3 authors at 1 institution in 1 country.

Thomas A AngelovichCentre for Biomedical Research, Burnet Institute, Melbourne, VIC, Australia.ORCID http://orcid.org/0000-0003-2069-0451
Anna C HearpsCentre for Biomedical Research, Burnet Institute, Melbourne, VIC, Australia.
Anthony JaworowskiCentre for Biomedical Research, Burnet Institute, Melbourne, VIC, Australia.
Burnet Institute · AU

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Atherosclerosis is the leading cause of cardiovascular disease and is both a metabolic and inflammatory disease. Two models describe early events initiating atherosclerotic plaque formation, whereby foam cells form in response to hyperlipidaemia or inflammation-associated stimuli. Although these models are inextricably linked and not mutually exclusive, identifying the unique contribution of each in different disease settings remains an important question. Circulating monocytes are key mediators of atherogenesis in both models as precursors to lipid-laden foam cells formed in response to either excess lipid deposition in arteries, signalling via pattern-associated molecular patterns or a combination of the two. In this review, we assess the role of monocytes in each model and discuss how key steps in atherogenesis may be targeted to enhance clinical outcomes in patients with chronic inflammatory disease.

Indexed as

AnimalsAtherosclerosisChronic DiseaseDisease Models, AnimalFoam CellsHumansInflammationLipid MetabolismMacrophage ActivationMonocytesPlaque, AtheroscleroticRisk FactorsToll-Like ReceptorsToll-Like Receptors

Identifiers

PMID25753272
OpenAlexW2088825420

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.