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Related Experiment Video

Updated: Sep 26, 2025

In Situ Immunofluorescent Staining of Autophagy in Muscle Stem Cells

In Situ Immunofluorescent Staining of Autophagy in Muscle Stem Cells

Published on: June 12, 2017

Autophagy guards tendon homeostasis.

Costanza Montagna^1,2,3,4, Rene B Svensson^5,6, Monika L Bayer^5,6

¹Institute of Sports Medicine Copenhagen, Department of Orthopedic Surgery, Copenhagen University Hospital-Bispebjerg and Frederiksberg, Copenhagen, Denmark. costanza.montagna@unicamillus.org.

Cell Death & Disease

|April 24, 2022

Summary

Autophagy, a cellular recycling process, is active in human tendons and regulates collagen production. Its activation impairs tendon biomechanical properties, suggesting a role in tendinopathy development.

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A Protocol to Acquire the Degenerative Tenocyte from Humans

A Protocol to Acquire the Degenerative Tenocyte from Humans

Published on: June 9, 2018

Area of Science:

Biomedical Engineering
Cellular Biology
Orthopedics

Background:

Tendons are crucial for movement, but the mechanisms regulating their matrix quality and the causes of tendinopathy remain unclear.
Autophagy is a key cellular process for maintaining tissue homeostasis in various tissues.
Understanding autophagy's role in tendons is essential for addressing tendinopathy.

Purpose of the Study:

To investigate the role of autophagy in human tendon physiology.
To determine if autophagy regulates the quality control of type I procollagen (PC1) secretion.
To examine the impact of autophagy modulation on tendon structure and function.

Main Methods:

Investigated autophagy activity in human tendon tissue in vivo.
Utilized three-dimensional tissue-engineered tendons to study the effects of pharmacological autophagy activation (mTOR inhibition).
Analyzed changes in collagen ultrastructure and biomechanical properties.

Main Results:

Provided in vivo evidence for active autophagy in human tendon tissue.
Demonstrated that ER-phagy (selective autophagy of the endoplasmic reticulum) regulates type I procollagen secretion.
Showed that pharmacological autophagy induction alters collagen fibril size and reduces mechanical strength in engineered tendons.

Conclusions:

Autophagy plays a critical role in tendon homeostasis by controlling type I procollagen quality.
Autophagy modulation impacts tendon ultrastructure and biomechanical integrity.
Findings suggest autophagy's involvement in the pathogenesis of injured tendons, offering potential therapeutic targets.