Evidence map›Paper›PMID 19759373›Full record

ReviewArteriosclerosis, thrombosis, and vascular biology2009

Regulation of the migration and survival of monocyte subsets by chemokine receptors and its relevance to atherosclerosis.

Emmanuel L Gautier, Claudia Jakubzick, Gwendalyn J Randolph

Open access · bronzeAbstract readReview
In one paragraph

Review in Arteriosclerosis, thrombosis, and vascular biology, 2009. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 113 papers.

0numbers the graph read from it
0cells of the map it votes in
113citing papers in PubMed
10.2field-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

113 citing papers in PubMed, 211 citations in OpenAlex.

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  10. The frequency of CD38Nature communications · 2024
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  13. Alpha-1 antitrypsin inhibits fractalkine-mediated monocyte-lung endothelial cell interactions.American journal of physiology. Lung cellular and molecular physiology · 2023
    Article
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  15. Article
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53 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

3 authors at 1 institution in 1 country.

Emmanuel L GautierDepartment of Gene and Cell Medicine, Mount Sinai School of Medicine, 1425 Madison Avenue, New York, NY 10029, USA.
Claudia Jakubzick
Gwendalyn J Randolph
Icahn School of Medicine at Mount Sinai · US

Funding

Molecular Regulation of Atherosclerosis Regression - RenewalR01HL084312 · NHLBI · NEW YORK UNIVERSITY SCHOOL OF MEDICINE · PI FISHER, EDWARD A · 2006 to 2024
$11.4M
Differentiation/migratory fate of monocyte-derived cellsR01AI049653 · NIAID · WASHINGTON UNIVERSITY · PI Gwendalyn J Randolph · 2000 to 2026
$4.6M
DIFFERENTIATION AND FUNCTION OF MONOCYTES AND MACROPHAGESR37AI049653 · NIAID · WASHINGTON UNIVERSITY · PI RANDOLPH, GWENDALYN J · 2016 to 2025
$4.3M
Pathways that regulate monocyte/dendritic cell migrationR01AI061741 · NIAID · WASHINGTON UNIVERSITY · PI RANDOLPH, GWENDALYN J · 2007 to 2011
$2.0M
NHLBI NIH HHS HL084312NHLBI NIH HHS R01 HL084312NIAID NIH HHS AI049653NIAID NIH HHS AI061741NIAID NIH HHS R01 AI049653NIAID NIH HHS R01 AI061741NIAID NIH HHS R37 AI049653
6 · The paper itself

Abstract

Monocytes are central mediators in the advance of atherosclerotic plaque, making them a natural therapeutic target for reducing disease burden. Here, we highlight recent advances in our current understanding of monocyte heterogeneity and its relevance to regulation of monocyte accumulation and function within atherosclerotic plaques. Differences that distinguish monocyte subsets include differential expression of chemokine receptors, especially CCR2 and CX3CR1. Ablation of expression of these 2 receptors (or their ligands) in mice has an additive inhibition on monocyte recruitment to atherosclerotic plaques. Moreover, simultaneously interfering with 3 key pathways--CCR2, CX3CR1, and CCR5--essentially abolishes atherosclerosis in mice. Here, we discuss how these chemokine receptors act at multiple points on at least 1 monocyte subset, regulating their mobilization from bone marrow, survival, or recruitment to plaques. Finally, we discuss how this knowledge may be useful clinically, emphasizing that CX3CR1 may in particular be a viable target for therapeutic manipulation of monocyte-derived cell fate in cardiovascular disease.

Indexed as

AnimalsAtherosclerosisCell MovementCell SurvivalChemokine CXCL16Chemokines, CXCCX3C Chemokine Receptor 1HumansMonocytesReceptors, CCR2Receptors, ChemokineReceptors, Oxidized LDLReceptors, ScavengerChemokine CXCL16Chemokines, CXCCX3C Chemokine Receptor 1CX3CR1 protein, humanCXCL16 protein, humanReceptors, CCR2Receptors, ChemokineReceptors, Oxidized LDLReceptors, Scavenger

Identifiers

PMID19759373
PMCPMC2782657
OpenAlexW2123811618

What OpenQuestion holds

Textmetadata
LicenceTDM
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.