Evidence map›Paper›PMID 24816217›Full record

ArticleJournal of molecular and cellular cardiology2014

CXCR4 blockade induces atherosclerosis by affecting neutrophil function.

Ilze Bot, Isabelle T M N Daissormont, Alma Zernecke, Gijs H M van Puijvelde, Birgit Kramp, Saskia C A de Jager, Judith C Sluimer, Marco Manca, Veronica Hérias, Marijke M Westra and 12 more

Open access · bronzeAbstract read
In one paragraph

Article in Journal of molecular and cellular cardiology, 2014. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 31 papers.

0numbers the graph read from it
0cells of the map it votes in
31citing papers in PubMed
3.6field-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

31 citing papers in PubMed, 62 citations in OpenAlex.

  1. Advances in GPCR-Targeted PET Radiotracer Patents (2020-2025).Pharmaceuticals (Basel, Switzerland) · 2026
    Review
  2. From incidental positron emission uptake toFrontiers in cardiovascular medicine · 2026
    Review
  3. Review
  4. Review
  5. Review
  6. Identification of common mechanisms and biomarkers for dermatomyositis and atherosclerosis based on bioinformatics analysis.Skin research and technology : official journal of International Society for Bioengineering and the Skin (ISBS) [and] International Society for Digital Imaging of Skin (ISDIS) [and] International Society for Skin Imaging (ISSI) · 2024
    Article
  7. Review
  8. Article
  9. Article
  10. Article
  11. Article
  12. Article
  13. Review
  14. Article
  15. Interleukin-17-Producing CD4Frontiers in cardiovascular medicine · 2021
    Article
  16. Article
  17. Article
  18. Article
  19. [European journal of nuclear medicine and molecular imaging · 2019
    Article
  20. 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

22 authors at 8 institutions in 4 countries.

Ilze BotDivision of Biopharmaceutics, Leiden Academic Centre for Drug Research, Leiden University, Leiden, The Netherlands. Electronic address: i.bot@lacdr.leidenuniv.nl.
Isabelle T M N DaissormontExperimental Vascular Pathology Group, Cardiovascular Research Institute Maastricht, University of Maastricht, Maastricht, The Netherlands.
Alma ZerneckeRudolf-Virchow-Center/DFG-Research Center for Experimental Biomedicine, University of Würzburg, Würzburg, Germany.
Gijs H M van PuijveldeDivision of Biopharmaceutics, Leiden Academic Centre for Drug Research, Leiden University, Leiden, The Netherlands.
Birgit KrampInstitute for Cardiovascular Prevention, Ludwig-Maximilians-Universität München, Munich, Germany.
Saskia C A de JagerDivision of Biopharmaceutics, Leiden Academic Centre for Drug Research, Leiden University, Leiden, The Netherlands.
Judith C SluimerExperimental Vascular Pathology Group, Cardiovascular Research Institute Maastricht, University of Maastricht, Maastricht, The Netherlands.
Marco MancaExperimental Vascular Pathology Group, Cardiovascular Research Institute Maastricht, University of Maastricht, Maastricht, The Netherlands.
Veronica HériasExperimental Vascular Pathology Group, Cardiovascular Research Institute Maastricht, University of Maastricht, Maastricht, The Netherlands.
Marijke M WestraDivision of Biopharmaceutics, Leiden Academic Centre for Drug Research, Leiden University, Leiden, The Netherlands.
Martine BotDivision of Biopharmaceutics, Leiden Academic Centre for Drug Research, Leiden University, Leiden, The Netherlands.
Peter J van SantbrinkDivision of Biopharmaceutics, Leiden Academic Centre for Drug Research, Leiden University, Leiden, The Netherlands.
Theo J C van BerkelDivision of Biopharmaceutics, Leiden Academic Centre for Drug Research, Leiden University, Leiden, The Netherlands.
Lishan SuDepartment of Microbiology & Immunology, Lineberger Comprehensive Cancer Center, Curriculum in Genetics and Molecular Biology School of Medicine, The University of North Carolina, Chapel Hill, NC 27599-7295.
Mona SkjellandDepartment of Neurology, Rikshospitalet University Hospital, University of Oslo, Norway.
Lars GullestadDepartment of Cardiology, Rikshospitalet University Hospital, University of Oslo, Norway.
Johan KuiperDivision of Biopharmaceutics, Leiden Academic Centre for Drug Research, Leiden University, Leiden, The Netherlands.
Bente HalvorsenDepartment of Internal Medicine, Rikshospitalet University Hospital, University of Oslo, Norway.
Paul AukrustDepartment of Internal Medicine, Rikshospitalet University Hospital, University of Oslo, Norway.
Rory R KoenenInstitute for Cardiovascular Prevention, Ludwig-Maximilians-Universität München, Munich, Germany.
Christian WeberInstitute for Cardiovascular Prevention, Ludwig-Maximilians-Universität München, Munich, Germany.
Erik A L BiessenDivision of Biopharmaceutics, Leiden Academic Centre for Drug Research, Leiden University, Leiden, The Netherlands; Experimental Vascular Pathology Group, Cardiovascular Research Institute Maastricht, University of Maastricht, Maastricht, The Netherlands.
Maastricht University · NLCentre for Human Drug Research · NLLeiden University · NLLudwig-Maximilians-Universität München · DEUniversity of Oslo · NOOslo University Hospital · NOUniversity of North Carolina at Chapel Hill · USUniversity of Würzburg · DE

Funding

HIV-1 Replication and Pathogenesis in the Human ThymusR01AI041356 · NIAID · UNIV OF NORTH CAROLINA CHAPEL HILL · PI SU, LISHAN · 1998 to 2007
$2.2M
RHOA EFFECTOR IN HIV-1 REPLICATION AND PATHOGENESISR01AI048407 · NIAID · UNIVERSITY OF NORTH CAROLINA CHAPEL HILL · PI SU, LISHAN · 2000 to 2004
$1.6M
HIV-1 Replication and Pathogenesis in vivoR01AI080432 · NIAID · UNIV OF NORTH CAROLINA CHAPEL HILL · PI SU, LISHAN · 2009 to 2012
$1.4M
Modulation of HIV-1 Replication and T Cell Activation by FoxP3R56AI048407 · NIAID · UNIV OF NORTH CAROLINA CHAPEL HILL · PI SU, LISHAN · 2007 to 2007
$363k
Genetic Analy. of Chemokine Receptors in T Cell Develop.R21AI053804 · NIAID · UNIVERSITY OF NORTH CAROLINA CHAPEL HILL · PI SU, LISHAN · 2002 to 2003
$361k
NIAID NIH HHS AI048407NIAID NIH HHS AI41356NIAID NIH HHS R01 AI041356NIAID NIH HHS R01 AI048407NIAID NIH HHS R01 AI080432NIAID NIH HHS R21 AI053804NIAID NIH HHS R56 AI048407
6 · The paper itself

Abstract

aimsThe SDF-1α/CXCR4 dyad was previously shown by us and others to be instrumental in intimal hyperplasia as well as early stage atherosclerosis. We here sought to investigate its impact on clinically relevant stages of atherosclerosis in mouse and man. METHODS AND

resultsImmunohistochemical analysis of CXCR4 expression in human atherosclerotic lesions revealed a progressive accumulation of CXCR4(+) cells during plaque progression. To address causal involvement of CXCR4 in advanced stages of atherosclerosis we reconstituted LDLr(-/-) mice with autologous bone marrow infected with lentivirus encoding SDF-1α antagonist or CXCR4 degrakine, which effects proteasomal degradation of CXCR4. Functional CXCR4 blockade led to progressive plaque expansion with disease progression, while also promoting intraplaque haemorrhage. Moreover, CXCR4 knockdown was seen to augment endothelial adhesion of neutrophils. Concordant with this finding, inhibition of CXCR4 function increased adhesive capacity and reduced apoptosis of neutrophils and resulted in hyperactivation of circulating neutrophils. Compatible with a role of the neutrophil CXCR4 in end-stage atherosclerosis, CXCR4 expression by circulating neutrophils was lowered in patients with acute cardiovascular syndromes.

conclusionIn conclusion, CXCR4 contributes to later stages of plaque progression by perturbing neutrophil function.

Indexed as

AnimalsAtherosclerosisBone Marrow CellsBone Marrow TransplantationCell AdhesionChemokine CXCL12Disease ProgressionEndothelial CellsFemaleGene Expression RegulationGenetic VectorsHemorrhageHumansLentivirusMiceMice, KnockoutChemokine CXCL12Proteasome Endopeptidase ComplexReceptors, CXCR4Receptors, LDLatherosclerosisCXCR4neutrophilsSDF-1αsenescence

Identifiers

PMID24816217
PMCPMC4418455
OpenAlexW2033993593

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.