ArticleOsteoarthritis and cartilage2023
Synovial fluid mitochondrial DNA concentration reflects the degree of cartilage damage after naturally occurring articular injury.
Article in Osteoarthritis and cartilage, 2023. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 7 papers.
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Who cites it
7 citing papers in PubMed, 18 citations in OpenAlex.
- Mitochondrial DNA released from pyroptotic synovial macrophages via DDIT3-mediated mitophagy aggravates osteoarthritis progression.Journal of orthopaedic translation · 2026Article
- PPARγ Agonism Modulates Synovial Macrophage and Cartilage Responses in an Equine Model of Synovial Inflammation-Implications for Joint Therapy.Biomolecules · 2025Article
- IRF1 regulation of ZBP1 links mitochondrial DNA and chondrocyte damage in osteoarthritis.Cell communication and signaling : CCS · 2024Article
- Molecular biomarker approaches to prevention of post-traumatic osteoarthritis.Nature reviews. Rheumatology · 2024Review
- Mitochondrial Fraction of Circulating Cell-Free DNA as an Indicator of Human Pathology.International journal of molecular sciences · 2024Article
- The role of mtDAMPs in the trauma-induced systemic inflammatory response syndrome.Frontiers in immunology · 2023Review
- Role of Mitochondrial Nucleic Acid Sensing Pathways in Health and Patho-Physiology.Frontiers in cell and developmental biology · 2022Review
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Authors and funding
4 authors at 1 institution in 1 country.
Funding
Abstract
objectiveTo evaluate mitochondrial DNA (mtDNA) release from injured chondrocytes and investigate the utility of synovial fluid mtDNA concentration in early detection of posttraumatic osteoarthritis.
methodWe measured mtDNA release using four models of osteoarthritis: in vitro interleukin-1β stimulation of cultured equine chondrocytes, ex vivo mechanical impact of bovine cartilage explants, in vivo mechanical impact of equine articular cartilage, and naturally occurring equine intraarticular fracture. In our in vivo model, one group was treated with an intraarticular injection of the mitoprotective peptide SS-31 following cartilage injury. mtDNA content was quantified using qPCR. For naturally occurring cases of joint injury, clinical data (radiographs, arthroscopic video footage) were scored for criteria associated with degenerative joint disease.
resultsChondrocytes released mtDNA in the acute time frame following inflammatory and mechanical cellular stress in vitro. mtDNA was increased in equine synovial fluid following experimental and naturally occurring injury to the joint surface. In naturally occurring posttraumatic osteoarthritis, we found a strong positive correlation between the degree of cartilage damage and mtDNA concentration (r = 0.80, P = 0.0001). Finally, impact-induced mtDNA release was mitigated by mitoprotective treatment.
conclusionChanges in synovial fluid mtDNA occur following joint injury and correlate with the severity of cartilage damage. Mitoprotection mitigates increases in synovial fluid mtDNA suggesting that mtDNA release may reflect mitochondrial dysfunction. Further investigation of mtDNA as a potentially sensitive marker of early articular injury and response to mitoprotective therapy is warranted.
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