Evidence map›Paper›PMID 10852110›Full record

ReviewImmunologic research2000

Interleukin-8 and its receptor CXCR2 in atherosclerosis.

W A Boisvert, L K Curtiss, R A Terkeltaub

Abstract readReview
PubMed Publisher
In one paragraph

Review in Immunologic research, 2000. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 46 papers.

0numbers the graph read from it
0cells of the map it votes in
46citing papers in PubMed
3.7field-weighted citation impact, top 7% 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

46 citing papers in PubMed, 143 citations in OpenAlex.

  1. Inherited human group IVA cytosolic phospholipase A2 deficiency abolishes platelet, endothelial, and leucocyte eicosanoid generation.FASEB journal : official publication of the Federation of American Societies for Experimental Biology · 2015
    Trial
  2. Identification of NR4A2 as a Potential Predictive Biomarker for Atherosclerosis.Combinatorial chemistry & high throughput screening · 2026
    Article
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  20. The SCFFBXO3 ubiquitin E3 ligase regulates inflammation in atherosclerosis.Journal of molecular and cellular cardiology · 2019
    Article
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 2 institutions in 1 country.

W A BoisvertDepartment of Immunology, The Scripps Research Institute, La Jolla, CA 92037, USA. boisvert@scripps.edu
L K Curtiss
R A Terkeltaub
Scripps Research Institute · USUniversity of California San Diego Medical Center · US

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

The participation of inflammatory cells in atherosclerosis is a well-known process that involves numerous molecules including chemotactic cytokines (chemokines) for their entry into the vessel wall. Although the C-C chemokine monocyte chemoattractant protein-1 and its receptor, CCR2, have been implicated in atherosclerosis, the role of the classic C-X-C chemokine, interleukin-8 (KC/growth-related oncogene alpha in mice) and its receptor CXCR2 has not been studied in the pathogenesis of atherosclerosis. Our research has shown that CXCR2 is strongly expressed on macrophages (Mphi) in atherosclerotic lesion. This CXCR2 expression is proatherogenic in that CXCR2 deficiency significantly reduces the progression of advanced atherosclerosis in mice. Although the mechanism still needs to be worked out, it appears that CXCR2 expression on lesion Mphi is essential for these cells to be retained in the lesion.

Indexed as

AnimalsArteriosclerosisHumansInterleukin-8MiceReceptors, ChemokineReceptors, InterleukinReceptors, Interleukin-8BInterleukin-8Receptors, ChemokineReceptors, InterleukinReceptors, Interleukin-8B

Identifiers

PMID10852110
OpenAlexW2086044289

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.