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Updated: Dec 8, 2025
Biomechanical Testing of Murine Tendons
Published on: October 15, 2019
Assessment of Mitochondrial Dysfunction in a Murine Model of Supraspinatus Tendinopathy
Xueying Zhang1,2, Susumu Wada1, Ying Zhang1
1Orthopedic Soft Tissue Research Program, Hospital for Special Surgery, New York, NY.
Background:
The purpose of this study was to assess mitochondrial dysfunction in a murine model of supraspinatus tendinopathy.
Methods:
Eighty-four mice (168 limbs) were included in the study. Supraspinatus tendinopathy was induced by inserting a microsurgical clip in the subacromial space of 63 mice bilaterally (126 limbs). Forty-two of these limbs were harvested at 4 weeks postoperatively, 42 underwent clip removal at 4 weeks after the initial procedure and were harvested at 2 weeks, and 42 underwent clip removal at 4 weeks and were harvested at 4 weeks. Forty-two limbs in the remaining 21 mice did not undergo surgical intervention and were utilized as the control group. Outcomes included biomechanical, histological, gene expression, superoxide dismutase (SOD) activity, and transmission electron microscopy (TEM) analyses.
Results:
Radiographs confirmed stable clip position in the subacromial space at 4 weeks. Biomechanical testing demonstrated a 60% decrease in failure force of the supraspinatus tendons at 4 weeks compared with the control group. The failure force gradually increased at 2 and 4 weeks after clip removal. Histological analysis demonstrated inflammation surrounding the tendon with higher modified Bonar scores at 4 weeks after clip placement followed by gradual improvement following clip removal. The expression of mitochondrial-related genes was decreased at 4 weeks after clip placement and then significantly increased after clip removal. SOD activity decreased significantly at 4 weeks after clip placement but increased following clip removal. TEM images demonstrated alterations in morphology and the number of mitochondria and cristae at 4 weeks after clip placement with improvement after clip removal.
Conclusions:
Mitochondrial dysfunction appears to be associated with the development of tendinopathy.
Clinical Relevance:
Mitochondrial protection may offer a potential strategy for delaying the development of tendinopathy and promoting tendon healing.
Insights
Mitochondrial dysfunction is linked to supraspinatus tendinopathy development. Protecting mitochondria may help delay tendinopathy and promote tendon healing.
Area of Science:
- Orthopedics
- Cell Biology
- Biomedical Engineering
Background:
- Supraspinatus tendinopathy is a common shoulder injury.
- Mitochondrial dysfunction is implicated in various degenerative conditions.
Purpose of the Study:
- To investigate mitochondrial dysfunction in a murine model of supraspinatus tendinopathy.
- To explore the role of mitochondria in the pathogenesis of this condition.
Main Methods:
- Induction of supraspinatus tendinopathy in mice using a subacromial clip.
- Assessment of biomechanical properties, histology, gene expression, superoxide dismutase (SOD) activity, and transmission electron microscopy (TEM).
- Evaluation at various time points post-clip placement and post-clip removal.
Main Results:
- Tendinopathy induced a significant decrease in supraspinatus tendon failure force and increased inflammation.
- Mitochondrial dysfunction was evidenced by decreased mitochondrial gene expression, reduced SOD activity, and altered mitochondrial morphology.
- These changes showed improvement following clip removal, indicating a reversible process.
Conclusions:
- Mitochondrial dysfunction is associated with the development of supraspinatus tendinopathy.
- Targeting mitochondrial function may be a therapeutic strategy for tendinopathy.
