Evidence map›Paper›PMID 23974513›Full record

ReviewActa pharmacologica Sinica2013

Chemokines and atherosclerosis: focus on the CX3CL1/CX3CR1 pathway.

Stavros Apostolakis, Demetrios Spandidos

Open access · bronzeAbstract readReview
In one paragraph

Review in Acta pharmacologica Sinica, 2013. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 73 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
73citing papers in PubMed, 1 pooled it
2.8field-weighted citation impact, top 9% 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

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

  1. Pooled it
  2. Trial
  3. Trial
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  5. Article
  6. The CX3CL1-CX3CR1 axis in HIV-associated inflammation and cardiometabolic disease.American journal of physiology. Regulatory, integrative and comparative physiology · 2026
    Review
  7. Article
  8. Article
  9. Mitigating atherosclerosis: Integrating vaccines with gene targets.American heart journal plus : cardiology research and practice · 2025
    Review
  10. Impaired endothelial cell-derived CX3CL1-mediated macrophage efferocytosis in hypertrophic cardiomyopathy based on multi-omics analysis.Inflammation research : official journal of the European Histamine Research Society ... [et al.] · 2025
    Article
  11. Article
  12. Article
  13. Review
  14. Review
  15. Article
  16. Review
  17. Article
  18. Article
  19. Article
  20. Mechanism of efferocytosis in atherosclerosis.Journal of molecular medicine (Berlin, Germany) · 2024
    Review

13 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

2 authors at 1 institution in 1 country.

Stavros ApostolakisDepartment of Clinical Virology, Faculty of Medicine, University of Crete, Heraklion, Crete, Greece.
Demetrios Spandidos
University of Crete · GR

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Atherosclerosis is currently considered an inflammatory disease. Much attention has been focused on the potential role of inflammatory mediators as prognostic/diagnostic markers or therapeutic targets of atherosclerotic cardiovascular disease. CX3CL1 (or fractalkine) is a structurally and functionally unique chemokine with a well documented role in atherosclerosis. In its membrane bound form it promotes the firm adhesion of rolling leucocytes onto the vessel wall, while in its soluble form it serves as a potent chemoattractant for CX3CR1-expressing cells. Additionally, CX3CL1 exerts cytotoxic effects on the endothelium as well as anti-apoptotic and proliferative effects on vascular cells, affecting the context and stability of the atherosclerotic plaque. Studies on animal models have shown that the blockade of the CX3CL1/CX3CR1 pathway ameliorates the severity of atherosclerosis, while genetic epidemiology has confirmed that a genetically-defined less active CX3CL1/CX3CR1 pathway is associated with a reduced risk of atherosclerotic disease in humans. Although several studies support an important pathogenic role of CX3CL1/CX3CR1 in atherogenesis and plaque destabilization, this does not necessarily suggest that this pathway is a suitable therapeutic target or that CX3CL1 can serve as a prognostic/diagnostic biomarker. Further studies on the CX3CL1/CX3CR1 chemokine pathway are clearly warranted to justify the clinical relevance of its role in atherosclerosis.

Indexed as

AnimalsAtherosclerosisBiomarkersChemokine CX3CL1Disease Models, AnimalGenetic Predisposition to DiseaseHumansInflammation MediatorsMolecular EpidemiologyPrognosisSeverity of Illness IndexBiomarkersChemokine CX3CL1CX3CL1 protein, humanInflammation Mediators

Identifiers

PMID23974513
PMCPMC4002164
OpenAlexW2141307898

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.