ArticleJSES international2026
Mitochondria dysfunction and increased expression of WNT5A and BNIP3 in tenocytes obtained from patients with tendinopathy.
Article in JSES international, 2026. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Not yet cited in PubMed.
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Abstract
Background: Tendinopathy is a significant source of pain and functional impairment, with contributions from various extrinsic and intrinsic factors. Prior studies have demonstrated the role of mitochondria (MT) dysfunction in a murine model of supraspinatus tendinopathy, with improvement in tendon structure following treatment with the mitochondrial protectant agent Szeto-Schiller-31 (elamipretide). However, there is very little information available on mitochondrial function in human tendinopathy. The purpose of this study is to compare MT function in human tenocytes obtained from pathologic tendons of patients with tendinopathy and normal tendons and to identify potential target genes for the treatment of tendinopathy. Methods: Samples of degenerative tendons from the upper extremity (biceps tendon [n = 7], rotator cuff [n = 4], and extensor carpi radialis brevis tendon [n = 2]; total n = 13) and normal tendons from the lower extremity (hamstring [n = 4], patellar [n = 3], and quadriceps [n = 2]; total n = 9) were collected during surgeries. Cell viability, ultrastructural morphology (using transmission electron microscopy), differentiation potential (adipogenesis and osteogenesis), MT membrane polarity, production of reactive oxygen species, and gene expression profile (using NanoString and quantitative real-time polymerase chain reaction (qRTPCR)) were analyzed. Results: Tenocytes from normal tendons exhibited higher colony formation potential ( Conclusion: Our results confirm MT dysfunction in the degenerative group, as reported in previous studies. The upregulation of the WNT5A and BNIP3 expression was confirmed by both Nanostring and qRT-PCR.
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