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Related Experiment Video

Updated: Jul 7, 2026

Engineering Tendon Assembloids to Probe Cellular Crosstalk in Disease and Repair
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Engineering Tendon Assembloids to Probe Cellular Crosstalk in Disease and Repair

Published on: March 22, 2024

Tendinopathy--from basic science to treatment.

Graham Riley1

  • 1Soft Tissue Research Group, School of Biological Sciences, University of East Anglia, Norwich NR4 7TJ, UK. graham.riley@uea.ac.uk

Nature Clinical Practice. Rheumatology
|February 1, 2008
PubMed
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Chronic tendon pathology (tendinopathy) involves altered matrix remodeling and molecular changes. Increased metalloproteinases like ADAM-12 and MMP-23 are observed, but their specific roles require further investigation for targeted therapies.

Area of Science:

  • Biochemistry
  • Cell Biology
  • Orthopedics

Background:

  • Tendinopathy is a common yet challenging condition.
  • Tendon matrix composition includes type I collagen, minor collagens, proteoglycans, and glycoproteins.
  • Tenocytes maintain the tendon matrix through continuous remodeling.

Purpose of the Study:

  • To investigate the molecular changes associated with chronic tendon pathology.
  • To explore the role of matrix remodeling and specific enzymes in tendinopathy.
  • To identify potential molecular targets for therapeutic intervention.

Main Methods:

  • Analysis of molecular changes in tendon matrix composition.
  • Assessment of tenocyte activity and matrix remodeling rates.
  • Examination of metalloproteinase enzyme expression in tendinopathy.

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A Protocol to Acquire the Degenerative Tenocyte from Humans
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Last Updated: Jul 7, 2026

Engineering Tendon Assembloids to Probe Cellular Crosstalk in Disease and Repair
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Published on: March 22, 2024

A Passive Ankle Dorsiflexion Testing System for an In Vivo Model of Overuse-induced Tendinopathy
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A Passive Ankle Dorsiflexion Testing System for an In Vivo Model of Overuse-induced Tendinopathy

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A Protocol to Acquire the Degenerative Tenocyte from Humans
09:25

A Protocol to Acquire the Degenerative Tenocyte from Humans

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Main Results:

  • Tendinopathy is linked to altered matrix remodeling.
  • Key molecular alterations include increased expression of type III collagen, fibronectin, tenascin C, aggrecan, and biglycan.
  • Elevated levels of ADAM-12 and MMP-23 metalloproteinases are observed in painful tendinopathy.

Conclusions:

  • Molecular changes in tendinopathy may represent repair or adaptation to mechanical loading.
  • The precise role of ADAM-12 and MMP-23 in tendon pathology remains to be elucidated.
  • Further research is needed to identify specific molecular targets for effective tendinopathy treatments.