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Evaluation of SS-31 as a Potential Strategy for Tendinopathy Treatment: An In Vitro Model
Xueying Zhang1,2, Ying Zhang1, Meng Zhang1
1Orthopedic Soft Tissue Research Program, Hospital for Special Surgery, New York, New York, USA.
Mitochondrial dysfunction is present in supraspinatus tendinopathy. The drug SS-31 (elamipretide) improved mitochondrial function and morphology in patient-derived tenocytes, suggesting potential for tendinopathy treatment.
Area of Science:
- Biomedical Science
- Cell Biology
- Mitochondrial Medicine
Background:
- Mitochondrial dysfunction is implicated in supraspinatus tendinopathy.
- SS-31 (elamipretide) is known to enhance mitochondrial function.
- The therapeutic potential of SS-31 for tendinopathy remains unexplored.
Purpose of the Study:
- To investigate the effect of SS-31 on mitochondrial function in human tenocytes from patients with tendinopathy.
- To determine if SS-31 can reverse mitochondrial dysfunction in degenerative tenocytes.
Main Methods:
- Human tenocytes from healthy and tendinopathic donors were cultured.
- Tenocytes were treated with SS-31 (1μM) for 72 hours.
- Mitochondrial potential, morphology, ROS, SOD activity, gene expression, and cell viability were assessed.
Main Results:
- Degenerative tenocytes showed increased mitochondrial depolarization and altered morphology, which improved with SS-31 treatment.
- SS-31 treatment increased superoxidative dismutase activity and reduced upregulated matrix metalloproteinase-1 and fatty acid-binding protein 4 gene expression.
- Cell viability in degenerative tenocytes showed a slight improvement with SS-31.
Conclusions:
- Tenocytes from degenerative tendons exhibit mitochondrial dysfunction.
- SS-31 demonstrates potential to improve mitochondrial function and morphology in tendinopathy.
- SS-31 may serve as a therapeutic agent for promoting tendinopathy healing.
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