Evidence map›Paper›PMID 34081345›Full record

ArticleJournal of orthopaedic research : official publication of the Orthopaedic Research Society2022

Untargeted metabolomics analysis identifies creatine, myo-inositol, and lipid pathway modulation in a murine model of tendinopathy.

Katie J Sikes, Anna McConnell, Natalie Serkova, Brian Cole, David Frisbie

Open access · greenAbstract read
In one paragraph

Article in Journal of orthopaedic research : official publication of the Orthopaedic Research Society, 2022. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 10 papers.

0numbers the graph read from it
0cells of the map it votes in
10citing papers in PubMed
1.8field-weighted citation impact, top 17% 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

10 citing papers in PubMed, 15 citations in OpenAlex.

  1. Article
  2. Article
  3. Tendinopathy: The Interplay between Mechanical Stress, Inflammation, and Vascularity.Advanced science (Weinheim, Baden-Wurttemberg, Germany) · 2025
    Review
  4. Metabolomics: Uncovering Insights into Obesity and Diabetes.International journal of molecular sciences · 2025
    Article
  5. Review
  6. Article
  7. Review
  8. Article
  9. Article
  10. Review
4 · The record

Corrections and comments

5 · Who and what money

Authors and funding

5 authors at 3 institutions in 1 country.

Katie J SikesDepartment of Clinical Sciences, Orthopaedic Research Center, Colorado State University, Fort Collins, Colorado, USA.ORCID 0000-0002-3750-4777
Anna McConnellDepartment of Clinical Sciences, Orthopaedic Research Center, Colorado State University, Fort Collins, Colorado, USA.
Natalie SerkovaDepartment of Radiology, University of Colorado Denver, Denver, Colorado, USA.
Brian ColeDepartment of Orthopaedic Surgery, Rush University Medical Center, Chicago, Illinois, USA.
David FrisbieDepartment of Clinical Sciences, Orthopaedic Research Center, Colorado State University, Fort Collins, Colorado, USA.
Colorado State University · USRush University Medical Center · USUniversity of Denver · US

Funding

University of Colorado Cancer Center Support Grant - Lung Cancer Patient-Derived Xenografts with Autologous Human Immune SystemsP30CA046934 · NCI · UNIVERSITY OF COLORADO DENVER · PI James V Degregori · 1988 to 2026
$117.0M
NIH Prior Approval Process ProfessionalUL1TR002535 · NCATS · UNIVERSITY OF COLORADO DENVER · PI SOKOL, RONALD J. · 2018 to 2022
$51.1M
Bruker 9.4T/ 20cm BioSpec MR Scanner for Colorado Animal Imaging Shared ResourcesS10OD023485 · OD · UNIVERSITY OF COLORADO DENVER · PI SERKOVA, NATALIE J. · 2017 to 2017
$2.0M
NCATS NIH HHS UL1 TR002535NCI NIH HHS P30 CA046934NIH HHS S10 OD023485
6 · The paper itself

Abstract

Tendinopathy has been broadly characterized as alterations in cell proliferation, extracellular matrix turnover/synthesis, and inflammatory alterations. However, the underlying glucose metabolism pathways which contribute to these responses have not been well explored. The potential link between glucose metabolism and tendon pathology is interesting from a global standpoint since the development of spontaneous tendinopathy is associated with systemic metabolic disorders including diabetes mellitus. Therefore, the overarching goal of this study was to understand the potential pathogenic role of glucose metabolism-driven mechanisms in the development of tendinopathy. To test this, we have utilized an untargeted metabolomics approach to discover pathways which may be altered following tendinopathic injury and treadmill running in an established murine model of TGF-β1 induced tendinopathy. While specific tendon glucose alterations were not observed via metabolomics or

Indexed as

CreatineTendinopathyAnimalsDisease Models, AnimalFluorodeoxyglucose F18GlucoseHumansInositolLipidsMetabolomicsMicePositron Emission Tomography Computed TomographyX-Ray MicrotomographyCreatineFluorodeoxyglucose F18GlucoseInositolLipidscreatinelipidsmetabolomicsmyo-inositoltendinopathy

Identifiers

PMID34081345
PMCPMC8639838
OpenAlexW3164850805

What OpenQuestion holds

Textmetadata
LicenceTDM
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.