ArticleJournal of orthopaedic research : official publication of the Orthopaedic Research Society2018
Mitochondrial dysfunction is an acute response of articular chondrocytes to mechanical injury.
Article in Journal of orthopaedic research : official publication of the Orthopaedic Research Society, 2018. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 47 papers.
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Who cites it
47 citing papers in PubMed, 71 citations in OpenAlex.
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- Therapeutic effect of mitochondrial transfer on bone tissue diseases: treatment strategy of mitochondrial transplantation and delivery technology.Journal of orthopaedic translation · 2026Review
- Loss of connexin 43 in cartilage causes mitochondrial dysfunction and accelerates post-traumatic osteoarthritis progression.bioRxiv : the preprint server for biology · 2026Article
- Oxygen tension alters cartilage redox balance in response to traumatic impact.Bone & joint research · 2026Article
- Fibroblast-derived exosomes induce macrophage pyroptosis to mediate orthodontic bone remodeling through the mtDNA/NLRP3 axis.Journal of nanobiotechnology · 2026Article
- Mitochondria dysfunction and increased expression of WNT5A and BNIP3 in tenocytes obtained from patients with tendinopathy.JSES international · 2026Article
- From mechanical triggering to metabolic-inflammatory driving: a new paradigm of knee osteoarthritis pathogenesis.Frontiers in immunology · 2026Review
- Multiple strategies, one mission: mesenchymal stromal cell-based mechanisms of action in osteoarthritis.Frontiers in cell and developmental biology · 2026Review
- Beyond cartilage degeneration: osteoarthritis as a systems failure of inflammation regulation.Frontiers in medicine · 2026Article
- Time-dependent computational model of post-traumatic osteoarthritis to estimate how mechanoinflammatory mechanisms impact cartilage aggrecan content.PLoS computational biology · 2025Article
- Optical Redox Imaging Predicts Post-Loading Cartilage Mitochondrial Membrane Potential.Annals of biomedical engineering · 2025Article
- Bioactive Therapies for Degenerative Disc Disease: Challenges and Innovations.World neurosurgery · 2025Article
- In Vitro Impact Model to Generate Sublethal Chondrocyte Injury in Bovine Cartilage Explants.Journal of visualized experiments : JoVE · 2025Article
- A Molecular Chemical Perspective: Mitochondrial Dynamics Is Not a Bystander of Cartilage Diseases.ACS pharmacology & translational science · 2025Review
- Impact of Abnormal Mechanical Stress on Chondrocyte Death in Osteoarthritis.Medical science monitor : international medical journal of experimental and clinical research · 2025Review
- The gut microbiome and osteoarthritis.Reumatologia · 2025Review
- Connexin 43 regulates intercellular mitochondrial transfer from human mesenchymal stromal cells to chondrocytes.Stem cell research & therapy · 2024Article
- A Reproducible Cartilage Impact Model to Generate Post-Traumatic Osteoarthritis in the Rabbit.Journal of visualized experiments : JoVE · 2023Article
- Inflammatory mechanisms in post-traumatic osteoarthritis: a role for CaMKK2.Immunometabolism (Cobham, Surrey) · 2023Review
- Synovial fluid mitochondrial DNA concentration reflects the degree of cartilage damage after naturally occurring articular injury.Osteoarthritis and cartilage · 2023Article
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Authors and funding
4 authors at 1 institution in 1 country.
Funding
Abstract
Mitochondrial (MT) dysfunction is known to occur in chondrocytes isolated from end-stage osteoarthritis (OA) patients, but the role of MT dysfunction in the initiation and early pathogenesis of post-traumatic OA (PTOA) remains unclear. The objective of this study was to investigate chondrocyte MT function immediately following mechanical injury in cartilage, and to determine if the response to injury differed between a weight bearing region (medial femoral condyle; MFC) and a non-weight bearing region (distal patellofemoral groove; PFG) of the same joint. Cartilage was harvested from the MFC and PFG of 10 neonatal bovids, and subjected to injurious compression at varying magnitudes (5-17 MPa, 5-34 GPa/s) using a rapid single-impact model. Chondrocyte MT respiratory function, MT membrane polarity, chondrocyte viability, and cell membrane damage were assessed in situ. Cartilage impact resulted in MT depolarization and impaired MT respiratory function within 2 h of injury. Cartilage from a non-weight bearing region of the joint (PFG) was more sensitive to impact-induced MT dysfunction and chondrocyte death than cartilage from a weight-bearing surface (MFC). Our findings suggest that MT dysfunction is an acute response of chondrocytes to cartilage injury, and that MT may play a key mechanobiological role in the initiation and early pathogenesis of PTOA. CLINICAL SIGNIFICANCE: Direct therapeutic targeting of MT function in the early post-injury time frame may provide a strategy to block perpetuation of tissue damage and prevent the development of PTOA. © 2017 Orthopaedic Research Society. Published by Wiley Periodicals, Inc. J Orthop Res 36:739-750, 2018.
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