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Updated: Aug 14, 2026
Engineering Tendon Assembloids to Probe Cellular Crosstalk in Disease and Repair
Published on: March 22, 2024
Umbilical cord-derived mitochondrial transplantation restores tendon structure and function in a preclinical model of
Da-Yoon Kim1, Mi Jin Kim1, Min-Jeong Park1
1Departments of Bio-convergence Science and Life Sciences, CHA University, Seongnam, 13488, Republic of Korea.
Background:
Achilles tendinopathy is a degenerative musculoskeletal disorder for which disease-modifying therapies remain limited, largely due to the inability of current interventions to directly restore cellular bioenergetic function. Emerging evidence has identified mitochondrial dysfunction as a central contributor to tendon degeneration, highlighting mitochondria as a potential therapeutic target. Here, we evaluated umbilical cord-derived mitochondria (UC-MT) as a dose-defined, cell-free therapeutic strategy for tendinopathy.
Methods:
UC-MT were isolated from human umbilical cord-derived mesenchymal stem cells and characterized for mitochondrial integrity and bioenergetic activity. Therapeutic efficacy was evaluated in vitro using TNF-α-induced human tenocyte injury models and in vivo in a collagenase-induced rat model of Achilles tendinopathy. Dose-response effects were systematically assessed (5, 10, and 20 µg), and mitochondrial function, metabolic profiles, extracellular matrix remodeling, and functional recovery were analyzed using integrated molecular, histological, and functional assays, including transcriptomic and metabolomic profiling.
Results:
UC-MT treatment significantly restored mitochondrial membrane potential, ATP production, and respiratory complex activity in injured tenocytes, accompanied by attenuation of inflammatory signalling. Among the tested doses, 10 µg UC-MT consistently produced the most robust therapeutic effects across mitochondrial, metabolic, and structural outcome measures. In vivo, UC-MT administration improved tendon histoarchitecture, collagen organization, and functional performance, while integrated multi-omics analyses revealed coordinated metabolic reprogramming, including restoration of mitochondrial complex I-linked bioenergetic pathways.
Conclusions:
Taken together, these findings position UC-MT as a dose-defined, cell-free therapeutic modality with translational potential for tendon regeneration. By directly targeting mitochondrial dysfunction, UC-MT restores mitochondrial bioenergetics and supports tendon regeneration in preclinical models of tendinopathy.
