Evidence map›Paper›PMID 23599431›Full record

Trial reportThe Journal of biological chemistry2013

Induction of C-X-C chemokine receptor type 7 (CXCR7) switches stromal cell-derived factor-1 (SDF-1) signaling and phagocytic activity in macrophages linked to atherosclerosis.

Wanshu Ma, Yiwei Liu, Nicholas Ellison, Jianzhong Shen

Open access · hybridAbstract readClinical Trial
In one paragraph

Trial report in The Journal of biological chemistry, 2013. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 45 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
45citing papers in PubMed, 1 pooled it
4.4field-weighted citation impact, top 5% 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

45 citing papers in PubMed, 1 synthesis or guideline pooled it, 80 citations in OpenAlex.

  1. Pooled it
  2. Article
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  4. Active Substances from the Micro-Immunotherapy Medicine 2LC1International journal of molecular sciences · 2025
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  12. αProceedings of the National Academy of Sciences of the United States of America · 2022
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  17. Article
  18. Article
  19. Where the Action Is-Leukocyte Recruitment in Atherosclerosis.Frontiers in cardiovascular medicine · 2021
    Review
  20. Review
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 1 institution in 1 country.

Wanshu MaDivision of Pharmacology, Department of Pharmacal Sciences, Harrison School of Pharmacy, Auburn University, Auburn, Alabama 36849, USA.
Yiwei Liu
Nicholas Ellison
Jianzhong Shen
Auburn University · US

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

The discovery of CXCR7 as a new receptor for SDF-1 places many previously described SDF-1 functions attributed to CXCR4 in question, though whether CXCR7 acts as a signaling or "decoy" receptor has been in debate. It is known that CXCR7 is not expressed in normal blood leukocytes; however, the potential role of leukocyte CXCR7 in disease states has not been addressed. The aim of this study was to determine the expression and function of macrophage CXCR7 linked to atherosclerosis. Here, we show that CXCR7 was detected in macrophage-positive area of aortic atheroma of ApoE-null mice, but not in healthy aorta. During monocyte differentiation to macrophages, CXCR7 was up-regulated at mRNA and protein levels, with more expression in M1 than in M2 phenotype. In addition, CXCR7 induction was associated with a SDF-1 signaling switch from the pro-survival ERK and AKT pathways in monocytes to the pro-inflammatory JNK and p38 pathways in macrophages. The latter effect was mimicked by a CXCR7-selective agonist TC14012 and abolished by siRNA knockdown of CXCR7. Furthermore, CXCR7 activation increased macrophage phagocytic activity, which was suppressed by CXCR7 siRNA silencing or by inhibiting either the JNK or p38 pathways, but was not affected by blocking CXCR4. Finally, activation of CXCR7 by I-TAC showed a similar signaling and phagocytic activity in macrophages with no detectable CXCR3. We conclude that CXCR7 is induced during monocyte-to-macrophage differentiation, which is required for SDF-1 and I-TAC signaling to JNK and p38 pathways, leading to enhanced macrophage phagocytosis, thus possibly contributing to atherogenesis.

Indexed as

MAP Kinase Signaling SystemPhagocytosisAnimalsAortaAtherosclerosisCell DifferentiationCell Line, TumorChemokine CXCL11Chemokine CXCL12FemaleGene Knockdown TechniquesHumansMacrophagesMaleMAP Kinase Kinase 4MiceACKR3 protein, humanChemokine CXCL11Chemokine CXCL12Cmkor1 protein, mouseCXCL11 protein, humanCxcl11 protein, mouseCXCL12 protein, humanCxcl12 protein, mouseCXCR3 protein, humanCxcr3 protein, mouseCXCR4 protein, humanCXCR4 protein, mouseMAP Kinase Kinase 4OligopeptidesProto-Oncogene Proteins c-aktReceptors, CXCRReceptors, CXCR3Receptors, CXCR4TC14012Cardiovascular DiseaseChemokinesMacrophagesMAP Kinases (MAPKs)Receptor Regulation

Identifiers

PMID23599431
PMCPMC3668710
OpenAlexW2137121530

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.