Evidence map›Paper›PMID 25791526›Full record

ReviewThe American journal of pathology2015

The role of formylated peptides and formyl peptide receptor 1 in governing neutrophil function during acute inflammation.

David A Dorward, Christopher D Lucas, Gavin B Chapman, Christopher Haslett, Kevin Dhaliwal, Adriano G Rossi

Open access · bronzeAbstract readReview
In one paragraph

Review in The American journal of pathology, 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 158 papers.

0numbers the graph read from it
0cells of the map it votes in
158citing papers in PubMed
10.5field-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

158 citing papers in PubMed, 254 citations in OpenAlex.

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98 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

6 authors at 4 institutions in 1 country.

David A DorwardMedical Research Council Centre for Inflammation Research, Queen's Medical Research Institute, University of Edinburgh Medical School, Edinburgh, United Kingdom. Electronic address: david.dorward@ed.ac.uk.
Christopher D LucasMedical Research Council Centre for Inflammation Research, Queen's Medical Research Institute, University of Edinburgh Medical School, Edinburgh, United Kingdom.
Gavin B ChapmanMedical Research Council Centre for Inflammation Research, Queen's Medical Research Institute, University of Edinburgh Medical School, Edinburgh, United Kingdom.
Christopher HaslettMedical Research Council Centre for Inflammation Research, Queen's Medical Research Institute, University of Edinburgh Medical School, Edinburgh, United Kingdom.
Kevin DhaliwalMedical Research Council Centre for Inflammation Research, Queen's Medical Research Institute, University of Edinburgh Medical School, Edinburgh, United Kingdom.
Adriano G RossiMedical Research Council Centre for Inflammation Research, Queen's Medical Research Institute, University of Edinburgh Medical School, Edinburgh, United Kingdom.
Medical Research Council · GBUniversity of Edinburgh · GBCentre for Inflammation Research · GBQueen's Medical Centre · GB

Funding

Medical Research Council G0601481Medical Research Council K013386/1Medical Research Council MR/J010901/1Medical Research Council MR/J014702/1Medical Research Council MR/K013386/1Wellcome TrustWellcome Trust WT094415Wellcome Trust WT096497
6 · The paper itself

Abstract

Neutrophil migration to sites of inflammation and the subsequent execution of multiple functions are designed to contain and kill invading pathogens. These highly regulated and orchestrated processes are controlled by interactions between numerous receptors and their cognate ligands. Unraveling and identifying those that are central to inflammatory processes may represent novel therapeutic targets for the treatment of neutrophil-dominant inflammatory disorders in which dysregulated neutrophil recruitment, function, and elimination serve to potentiate rather than resolve an initial inflammatory insult. The first G protein-coupled receptor to be described on human neutrophils, formyl peptide receptor 1 (FPR1), is one such receptor that plays a significant role in the execution of these functions through multiple intracellular signaling pathways. Recent work has highlighted important observations with regard to both receptor function and the importance and functional relevance of FPR1 in the pathogenesis of a range of both sterile and infective inflammatory conditions. In this review, we explore the multiple components of neutrophil migration and function in both health and disease, with a focus on the role of FPR1 in these processes. The current understanding of FPR1 structure, function, and signaling is examined, alongside discussion of the potential importance of FPR1 in inflammatory diseases suggesting that FPR1 is a key regulator of the inflammatory environment.

Indexed as

AnimalsChemotaxis, LeukocyteHumansInflammationNeutrophil ActivationNeutrophil InfiltrationNeutrophilsReceptors, Formyl PeptideReceptors, Formyl Peptide

Identifiers

PMID25791526
PMCPMC4419282
OpenAlexW2055477913

What Socratic 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 Socratic graph.