ArticleExperimental & molecular medicine2024
Mechanical overload-induced release of extracellular mitochondrial particles from tendon cells leads to inflammation in tendinopathy.
Article in Experimental & molecular medicine, 2024. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 11 papers.
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Who cites it
11 citing papers in PubMed, 13 citations in OpenAlex.
- Adipose-cartilage communication via EV-Mito-mtDNA signaling promotes osteoarthritis progression.Science advances · 2026Article
- Mitochondrial transfer and transplantation in tendon, ligament, and enthesis repair: current evidence, mechanistic rationale, and regenerative opportunities.Frontiers in cell and developmental biology · 2026Review
- Cyclic mechanical stimulation of TDCs improves tendon tissue maturationFrontiers in bioengineering and biotechnology · 2026Article
- The Novel Acromial Angle is associated with the severity of full-thickness rotator cuff tear: a retrospective radiographic study.Frontiers in medicine · 2026Article
- Exercise stress and tissue remodeling: advances in exosome-mediated RNA-RBP networks in musculoskeletal injury repair and functional recovery.Frontiers in genetics · 2026Review
- Review
- Open Challenges and Opportunities in Piezoelectricity for Tissue Regeneration.Advanced science (Weinheim, Baden-Wurttemberg, Germany) · 2025Review
- Computed microtomographic imaging of revascularization during healing of Achilles tendon injury.Journal of anatomy · 2025Article
- Beyond physical exhaustion: Understanding overtraining syndrome through the lens of molecular mechanisms and clinical manifestation.Sports medicine and health science · 2025Review
- Exploring molecular and cellular signaling pathways: Unraveling the pathogenesis of tendinopathy.Journal of orthopaedic translation · 2025Review
- Tendon mechanobiology in the context of tendon biofabrication.Frontiers in bioengineering and biotechnology · 2025Review
Corrections and comments
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Authors and funding
12 authors at 4 institutions in 3 countries.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Tendinopathy is one of the most common musculoskeletal diseases, and mechanical overload is considered its primary cause. However, the underlying mechanism through which mechanical overload induces tendinopathy has not been determined. In this study, we identified for the first time that tendon cells can release extracellular mitochondria (ExtraMito) particles, a subtype of medium extracellular particles (mEPs), into the environment through a process regulated by mechanical loading. RNA sequencing systematically revealed that oxygen-related reactions, extracellular particles, and inflammation were present in diseased human tendons, suggesting that these factors play a role in the pathogenesis of tendinopathy. We simulated the disease condition by imposing a 9% strain overload on three-dimensional mouse tendon constructs in our cyclic uniaxial stretching bioreactor. The three-dimensional mouse tendon constructs under normal loading with 6% strain exhibited an extended mitochondrial network, as observed through live-cell confocal laser scanning microscopy. In contrast, mechanical overload led to a fragmented mitochondrial network. Our microscopic and immunoblot results demonstrated that mechanical loading induced tendon cells to release ExtraMito particles. Furthermore, we showed that mEPs released from tendon cells overloaded with a 9% strain (mEP
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Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.