Evidence map›Paper›PMID 26443824›Full record

ArticleFASEB journal : official publication of the Federation of American Societies for Experimental Biology2016

CX3CR1 deficiency delays acute skeletal muscle injury repair by impairing macrophage functions.

Wanming Zhao, Haiyan Lu, Xingyu Wang, Richard M Ransohoff, Lan Zhou

Open access · greenAbstract read
In one paragraph

Article in FASEB journal : official publication of the Federation of American Societies for Experimental Biology, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 43 papers.

0numbers the graph read from it
0cells of the map it votes in
43citing papers in PubMed
2.1field-weighted citation impact, top 13% 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

43 citing papers in PubMed, 64 citations in OpenAlex.

  1. Article
  2. Article
  3. Exercise Impacts Liver Disease: Balancing Metabolic and Immune Homeostasis.International journal of biological sciences · 2026
    Review
  4. Article
  5. Article
  6. Review
  7. Review
  8. Chemogenetic manipulation of CX3CR1Molecular psychiatry · 2023
    Article
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  10. Article
  11. Review
  12. Article
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  14. Article
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  16. Article
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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

5 authors at 2 institutions in 1 country.

Wanming Zhao*Department of Neurology, Mount Sinai School of Medicine, New York, New York, USA; and Department of Neurosciences, Neuroinflammation Research Center, Cleveland Clinic, Cleveland, Ohio, USA.
Haiyan Lu*Department of Neurology, Mount Sinai School of Medicine, New York, New York, USA; and Department of Neurosciences, Neuroinflammation Research Center, Cleveland Clinic, Cleveland, Ohio, USA.
Xingyu Wang*Department of Neurology, Mount Sinai School of Medicine, New York, New York, USA; and Department of Neurosciences, Neuroinflammation Research Center, Cleveland Clinic, Cleveland, Ohio, USA.
Richard M Ransohoff*Department of Neurology, Mount Sinai School of Medicine, New York, New York, USA; and Department of Neurosciences, Neuroinflammation Research Center, Cleveland Clinic, Cleveland, Ohio, USA.
Lan Zhou*Department of Neurology, Mount Sinai School of Medicine, New York, New York, USA; and Department of Neurosciences, Neuroinflammation Research Center, Cleveland Clinic, Cleveland, Ohio, USA lan.zhou@mssm.edu.
Icahn School of Medicine at Mount Sinai · USCleveland Clinic · US

Funding

Targeting fibrocytes in Duchenne muscular dystrophyR01AR059702 · NIAMS · ICAHN SCHOOL OF MEDICINE AT MOUNT SINAI · PI ZHOU, LAN · 2011 to 2015
$1.9M
NIAMS NIH HHS R01 AR059702NIAMS NIH HHS R01AR059702
6 · The paper itself

Abstract

Adequate inflammatory response predominated by macrophage infiltration is essential to acute skeletal muscle injury repair. The majority of intramuscular macrophages express the chemokine receptor CX3CR1. We studied the role of CX3CR1 in regulating intramuscular macrophage number and function in acute injury repair by using a loss-of-function approach. Muscle injury repair was delayed in CX3CR1(GFP/GFP) mice as compared with wild-type (WT) controls. CX3CR1 was predominantly expressed by macrophages but not by myogenic cells or capillary endothelia cells in injured muscles. Intramuscular macrophage number and subset composition were not altered by CX3CR1 deficiency. Intramuscular macrophage phagocytosis function was impaired by CX3CR1 deficiency as demonstrated by increased number of necrotic fibers (+115%) and percentage of necrotic area (+204%) at 7 d, increased number of intramuscular neutrophils at 3 (+89%) but not 1 d, reduced number of phagocytosing macrophages (-12%) and phagocytosed beads within macrophages (-15%) in CX3CR1(GFP/GFP) mice as compared with WT controls. The mRNA expression of CD36 (-50%), CD14 (-43%), IGF-1 (-53%), and IL-6 (-40%) was reduced in CX3CR1-deficient macrophages as compared with WT controls. We conclude that CX3CR1 is important to acute skeletal muscle injury repair by regulating macrophage phagocytosis function and trophic growth factor production.

Indexed as

PhagocytosisRegenerationAnimalsCD36 AntigensCells, CulturedCX3C Chemokine Receptor 1Insulin-Like Growth Factor IInterleukin-6MacrophagesMiceMice, Inbred C57BLMuscle, SkeletalReceptors, ChemokineCD36 AntigensCX3C Chemokine Receptor 1Cx3cr1 protein, mouseInsulin-Like Growth Factor IInterleukin-6Receptors, ChemokinechemokineIGF-1monocyte recruitmentmuscle regenerationphagocytosis

Identifiers

PMID26443824
PMCPMC4684523
OpenAlexW2224835104

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.