Evidence map›Paper›PMID 24868552›Full record

ReviewBioMed research international2014

The multifaceted functions of CXCL10 in cardiovascular disease.

Pleunie van den Borne, Paul H A Quax, Imo E Hoefer, Gerard Pasterkamp

Open access · hybridAbstract readReview
In one paragraph

Review in BioMed research international, 2014. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 91 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
91citing papers in PubMed, 1 pooled it
3.4field-weighted citation impact, top 6% 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

91 citing papers in PubMed, 1 synthesis or guideline pooled it, 135 citations in OpenAlex.

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  20. The CXCL10-CXCR3 axis plays an important role in Kawasaki disease.Clinical and experimental immunology · 2024
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31 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

4 authors at 2 institutions in 1 country.

Pleunie van den BorneLaboratory of Experimental Cardiology, University Medical Center Utrecht, P.O. Box 85500, 3508 GA, Utrecht, The Netherlands.ORCID 0000-0002-4590-9985
Paul H A QuaxDepartment of Surgery, Leiden University Medical Center, P.O. Box 9600, 2300 RC, Leiden, The Netherlands ; Einthoven Laboratory of Experimental Vascular Medicine, Leiden University Medical Center, P.O. Box 9600, 2300 RC, Leiden, The Netherlands.
Imo E HoeferLaboratory of Experimental Cardiology, University Medical Center Utrecht, P.O. Box 85500, 3508 GA, Utrecht, The Netherlands ; Interuniversity Cardiology Institute of the Netherlands, P.O. Box 19258, 3501 DG, Utrecht, The Netherlands.
Gerard PasterkampLaboratory of Experimental Cardiology, University Medical Center Utrecht, P.O. Box 85500, 3508 GA, Utrecht, The Netherlands ; Interuniversity Cardiology Institute of the Netherlands, P.O. Box 19258, 3501 DG, Utrecht, The Netherlands.
University Medical Center Utrecht · NLLeiden University Medical Center · NL

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

C-X-C motif ligand 10 (CXCL10), or interferon-inducible protein-10, is a small chemokine belonging to the CXC chemokine family. Its members are responsible for leukocyte trafficking and act on tissue cells, like endothelial and vascular smooth muscle cells. CXCL10 is secreted by leukocytes and tissue cells and functions as a chemoattractant, mainly for lymphocytes. After binding to its receptor CXCR3, CXCL10 evokes a range of inflammatory responses: key features in cardiovascular disease (CVD). The role of CXCL10 in CVD has been extensively described, for example for atherosclerosis, aneurysm formation, and myocardial infarction. However, there seems to be a discrepancy between experimental and clinical settings. This discrepancy occurs from differences in biological actions between species (e.g. mice and human), which is dependent on CXCL10 signaling via different CXCR3 isoforms or CXCR3-independent signaling. This makes translation from experimental to clinical settings challenging. Furthermore, the overall consensus on the actions of CXCL10 in specific CVD models is not yet reached. The purpose of this review is to describe the functions of CXCL10 in different CVDs in both experimental and clinical settings and to highlight and discuss the possible discrepancies and translational difficulties. Furthermore, CXCL10 as a possible biomarker in CVD will be discussed.

Indexed as

Gene Expression RegulationAneurysmAnimalsAtherosclerosisBiomarkersCardiovascular DiseasesChemokine CXCL10Chemotactic FactorsHumansLeukocytesLymphocytesMiceMice, KnockoutMyocardial InfarctionSignal TransductionBiomarkersChemokine CXCL10Chemotactic FactorsCXCL10 protein, human

Identifiers

PMID24868552
PMCPMC4017714
OpenAlexW2112744681

What OpenQuestion holds

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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.