Evidence map›Paper›PMID 30883580›Full record

ArticlePloS one2019

Control of glucose metabolism is important in tenogenic differentiation of progenitors derived from human injured tendons.

Soutarou Izumi, Satoru Otsuru, Nobuo Adachi, Ngozi Akabudike, Motomi Enomoto-Iwamoto

Open access · goldAbstract read
In one paragraph

Article in PloS one, 2019. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 11 papers.

0numbers the graph read from it
0cells of the map it votes in
11citing papers in PubMed
1.7field-weighted citation impact, top 18% 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

11 citing papers in PubMed, 15 citations in OpenAlex.

  1. Article
  2. Moderate- and High-Speed Treadmill Running Exercise Have Minimal Impact on Rat Achilles Tendon.Journal of orthopaedic research : official publication of the Orthopaedic Research Society · 2025
    Article
  3. Review
  4. Review
  5. Article
  6. Article
  7. Inhibition of glucose use improves structural recovery of injured Achilles tendon in mice.Journal of orthopaedic research : official publication of the Orthopaedic Research Society · 2022
    Article
  8. Review
  9. Spectrum of Tendon Pathologies: Triggers, Trails and End-State.International journal of molecular sciences · 2020
    Review
  10. Small-Molecule Inhibition of Glucose Transporters GLUT-1-4.Chembiochem : a European journal of chemical biology · 2020
    Review
  11. 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

5 authors at 2 institutions in 2 countries.

Soutarou IzumiDepartment of Orthopaedics, University of Maryland, Baltimore, Baltimore, Maryland, United States of America.ORCID 0000-0003-1178-7171
Satoru OtsuruDepartment of Orthopaedics, University of Maryland, Baltimore, Baltimore, Maryland, United States of America.
Nobuo AdachiDepartment of Orthopaedic Surgery, Hiroshima University, Hiroshima, Japan.
Ngozi AkabudikeDepartment of Orthopaedics, University of Maryland, Baltimore, Baltimore, Maryland, United States of America.
Motomi Enomoto-IwamotoDepartment of Orthopaedics, University of Maryland, Baltimore, Baltimore, Maryland, United States of America.ORCID 0000-0002-9589-9607
University of Maryland, Baltimore · USHiroshima University · JP

Funding

Stimulation of Tendon Repair by Metabolic ModifiersR01AR070099 · NIAMS · UNIVERSITY OF MARYLAND BALTIMORE · PI ENOMOTO-IWAMOTO, MOTOMI · 2016 to 2020
$1.8M
NIAMS NIH HHS R01 AR070099
6 · The paper itself

Abstract

Glucose metabolism is altered in injured and healing tendons. However, the mechanism by which the glucose metabolism is involved in the pathogenesis of tendon healing process remains unclear. Injured tendons do not completely heal, and often induce fibrous scar and chondroid lesion. Because previous studies have shown that tendon progenitors play roles in tendon repair, we asked whether connective tissue progenitors appearing in injured tendons alter glucose metabolism during tendon healing process. We isolated connective tissue progenitors from the human injured tendons, obtained at the time of primary surgical repair of rupture or laceration. We first characterized the change in glucose metabolism by metabolomics analysis using [1,2-13C]-glucose using the cells isolated from the lacerated flexor tendon. The flux of glucose to the glycolysis pathway was increased in the connective tissue progenitors when they proceeded toward tenogenic and chondrogenic differentiation. The influx of glucose to the tricarboxylic acid (TCA) cycle and biosynthesis of amino acids from the intermediates of the TCA cycle were strongly stimulated toward chondrogenic differentiation. When we treated the cultures with 2-deoxy-D-glucose (2DG), an inhibitor of glycolysis, 2DG inhibited chondrogenesis as characterized by accumulation of mucopolysaccharides and expression of AGGRECAN. Interestingly, 2DG strongly stimulated expression of tenogenic transcription factor genes, SCLERAXIS and MOHAWK under both chondrogenic and tenogenic differentiation conditions. The findings suggest that control of glucose metabolism is beneficial for tenogenic differentiation of connective tissue progenitors.

Indexed as

AdultCell DifferentiationCells, CulturedChondrogenesisConnective Tissue CellsDeoxyglucoseGlucoseHumansMaleMiddle AgedStem CellsTendon InjuriesTendonsWound HealingYoung AdultDeoxyglucoseGlucose

Identifiers

PMID30883580
PMCPMC6422258
OpenAlexW2921919452

What OpenQuestion holds

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LicenceCC BY
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Registered trials

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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.