Evidence map›Paper›PMID 29696819›Full record

ArticlePhysiological reports2018

CXCL10 increases in human skeletal muscle following damage but is not necessary for muscle regeneration.

Michael R Deyhle, Paul S Hafen, Jacob Parmley, Coray N Preece, Marissa Robison, Jacob R Sorensen, Blake Jackson, Dennis L Eggett, Chad R Hancock, Robert D Hyldahl

Open access · goldAbstract read
In one paragraph

Article in Physiological reports, 2018. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 17 papers.

0numbers the graph read from it
0cells of the map it votes in
17citing papers in PubMed
1.7field-weighted citation impact, top 16% 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

17 citing papers in PubMed, 20 citations in OpenAlex.

  1. Review
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  7. Editorial: Chronic stress, telomeres and aging.Frontiers in endocrinology · 2024
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  8. Review
  9. Article
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  12. TNFα and IFNγ cooperate for efficient pro- to anti-inflammatory transition of macrophages during muscle regeneration.Proceedings of the National Academy of Sciences of the United States of America · 2022
    Article
  13. 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

10 authors at 1 institution in 1 country.

Michael R DeyhleDepartment of Exercise Sciences, Brigham Young University, Provo, Utah.
Paul S HafenDepartment of Exercise Sciences, Brigham Young University, Provo, Utah.
Jacob ParmleyDepartment of Exercise Sciences, Brigham Young University, Provo, Utah.
Coray N PreeceDepartment of Exercise Sciences, Brigham Young University, Provo, Utah.
Marissa RobisonDepartment of Exercise Sciences, Brigham Young University, Provo, Utah.
Jacob R SorensenDepartment of Exercise Sciences, Brigham Young University, Provo, Utah.
Blake JacksonDepartment of Exercise Sciences, Brigham Young University, Provo, Utah.
Dennis L EggettDepartment of Statistics, Brigham Young University, Provo, Utah.
Chad R HancockDepartment of Nutrition, Dietetics & Food Science, Brigham Young University, Provo, Utah.
Robert D HyldahlDepartment of Exercise Sciences, Brigham Young University, Provo, Utah.
Brigham Young University · US

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

CXCL10 is a chemokine for activated and memory T cells with many important immunological functions. We recently found that CXCL10 is upregulated in human muscle following contraction-induced damage. No information is available on the role of CXCL10 in the context of muscle damage or repair. In this study, we confirm that CXCL10 is elevated in human muscle at 2 and 3 days following damage and perform cell culture and animal studies to examine the role of CXCL10 in muscle repair. CXCL10 did not impact proliferation rates of human primary myoblasts but it did promote myogenic differentiation in vitro, suggesting a possible direct impact on muscle regeneration. To test if CXCL10 was dispensable for effective muscle regeneration in vivo, we measured functional and histological markers of muscle repair out to 14 days postmuscle injury caused by a myotoxin in wild-type (WT) mice and CXCL10 knockout (KO) mice. Between genotypes, no significant differences were found in loss or restoration of in situ muscle force, cross-sectional area of newly formed myofibers, or the number of embryonic myosin heavy chain-positive myofibers. In addition, KO animals were not deficient in T-cell accumulation in the damaged muscle following injury. Gene expression of the other two ligands (CXCL9 and 11) that bind to the same receptor as CXCL10 were also elevated in the damaged muscle of KO mice. Thus, other ligands may have compensated for the lack of CXCL10 in the KO mice. We conclude that CXCL10 is not necessary for effective muscle regeneration.

Indexed as

AdultCell DifferentiationChemokine CXCL10FemaleHumansMaleMuscle ContractionMuscle, SkeletalMyoblastsRegenerationUp-RegulationYoung AdultChemokine CXCL10chemokineCXCR3 ligandsinflammationIP-10T cell

Identifiers

PMID29696819
PMCPMC5917067
OpenAlexW2800087152

What OpenQuestion holds

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LicenceCC BY
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.