Evidence map›Paper›PMID 31792963›Full record

ArticleJournal of anatomy2020

Age-related changes of tendon fibril micro-morphology and gene expression.

Iris Ribitsch, Sinan Gueltekin, Marlies Franziska Keith, Kristina Minichmair, Christian Peham, Florien Jenner, Monika Egerbacher

Abstract read
In one paragraph

Article in Journal of anatomy, 2020. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 16 papers.

0numbers the graph read from it
0cells of the map it votes in
16citing papers in PubMed
–field-weighted citation impact
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

16 citing papers in PubMed.

  1. Article
  2. Article
  3. Article
  4. Article
  5. Tendon regeneration deserves better: focused review onFrontiers in bioengineering and biotechnology · 2025
    Review
  6. Article
  7. Article
  8. Review
  9. Review
  10. Article
  11. Article
  12. Large animal models for the study of tendinopathy.Frontiers in cell and developmental biology · 2022
    Review
  13. Tenascin-C: Friend or Foe in Lung Aging?Frontiers in physiology · 2021
    Article
  14. Article
  15. Review
  16. 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

7 authors.

Iris RibitschDepartment for Companion Animals and Horses, Veterm, University Equine Hospital, Vetmeduni Vienna, Vienna, Austria.ORCID 0000-0001-6618-2669
Sinan GueltekinDepartment for Companion Animals and Horses, Veterm, University Equine Hospital, Vetmeduni Vienna, Vienna, Austria.
Marlies Franziska KeithDepartment of Pathobiology, Unit of Histology and Embryology, Vetmeduni Vienna, Vienna, Austria.
Kristina MinichmairDepartment of Pathobiology, Unit of Histology and Embryology, Vetmeduni Vienna, Vienna, Austria.
Christian PehamDepartment for Companion Animals and Horses, Veterm, University Equine Hospital, Vetmeduni Vienna, Vienna, Austria.
Florien JennerDepartment for Companion Animals and Horses, Veterm, University Equine Hospital, Vetmeduni Vienna, Vienna, Austria.
Monika EgerbacherDepartment of Pathobiology, Unit of Histology and Embryology, Vetmeduni Vienna, Vienna, Austria.

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Aging is hypothesized to be associated with changes in tendon matrix composition which may lead to alteration of tendon material properties and hence propensity to injury. Altered gene expression may offer insights into disease pathophysiology and thus open new perspectives toward designing pathophysiology-driven therapeutics. Therefore, the current study aimed at identifying naturally occurring differences in tendon micro-morphology and gene expression of newborn, young and old horses. Age-related differences in the distribution pattern of tendon fibril thickness and in the expression of the tendon relevant genes collagen type 1 (Col1), Col3, Col5, tenascin-C, decorin, tenomodulin, versican, scleraxis and cartilage oligomeric matrix protein were investigated. A qualitative and quantitative gene expression and collagen fibril diameter analysis was performed for the most frequently injured equine tendon, the superficial digital flexor tendon, in comparison with the deep digital flexor tendon. Most analyzed genes (Col1, Col3, Col5, tenascin-C, tenomodulin, scleraxis) were expressed at a higher level in foals (age ≤ 6 months) than in horses of 2.75 years (age at which flexor tendons become mature in structure) and older, decorin expression increased with age. Decorin was previously reported to inhibit the lateral fusion of collagen fibrils, causing a thinner fibril diameter with increased decorin concentration. The results of this study suggested that reduction of tendon fibril diameters commonly seen in equine tendons with increasing age might be a natural age-related phenomenon leading to greater fibril surface areas with increased fibrillar interaction and reduced sliding at the fascicular/fibrillar interface and hence a stiffer interfascicular/interfibrillar matrix. This may be a potential reason for the higher propensity to tendinopathies with increasing age.

Indexed as

Gene ExpressionAge FactorsAgingAnimalsCollagenDecorinHorsesMembrane ProteinsTendonsCollagenDecorinMembrane Proteinsageanimal modeldecorinequinefibril diametergene expressionhorsetendon

Identifiers

PMID31792963
PMCPMC7083562

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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.