ArticleBiomechanics and modeling in mechanobiology2014
Strain-dependent oxidant release in articular cartilage originates from mitochondria.
Article in Biomechanics and modeling in mechanobiology, 2014. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 41 papers.
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Who cites it
41 citing papers in PubMed.
- Cellular mechanometabolism: stimuli and implications.EMBO reports · 2026Review
- MMP release following cartilage injury leads to collagen loss in intact tissue: A computational study.PLoS computational biology · 2026Article
- Influence of k-wire placement on impact mechanics and bone fracture in a rabbit model of cartilage injury.PloS one · 2026Article
- Time-dependent computational model of post-traumatic osteoarthritis to estimate how mechanoinflammatory mechanisms impact cartilage aggrecan content.PLoS computational biology · 2025Article
- Cartilage Redox Balance Is Influenced by Substrate Availability.Cartilage · 2025Article
- Mechanobiochemical finite element model to analyze impact-loading-induced cell damage, subsequent proteoglycan loss, and anti-oxidative treatment effects in articular cartilage.Biomechanics and modeling in mechanobiology · 2025Article
- A reciprocal relationship between mitochondria and lipid peroxidation determines the chondrocyte intracellular redox environment.Redox biology · 2024Article
- Synovial fluid mitochondrial DNA concentration reflects the degree of cartilage damage after naturally occurring articular injury.Osteoarthritis and cartilage · 2023Article
- Decreased SIRT1 Activity Is Involved in the Acute Injury Response of Chondrocytes to Ex Vivo Injurious Mechanical Overload.International journal of molecular sciences · 2023Article
- Multiscale In Silico Modeling of Cartilage Injuries.Advances in experimental medicine and biology · 2023Article
- Injury-related cell death and proteoglycan loss in articular cartilage: Numerical model combining necrosis, reactive oxygen species, and inflammatory cytokines.PLoS computational biology · 2023Article
- Extracellular biomolecular free radical formation during injury.Free radical biology & medicine · 2022Article
- Intra-Articular Adeno-Associated Virus-Mediated Proteoglycan 4 Gene Therapy for Preventing Posttraumatic Osteoarthritis.Human gene therapy · 2022Article
- Role of Mitochondria in Physiology of Chondrocytes and Diseases of Osteoarthritis and Rheumatoid Arthritis.Cartilage · 2021Review
- Intersections Between Mitochondrial Metabolism and Redox Biology Mediate Posttraumatic Osteoarthritis.Current rheumatology reports · 2021Review
- Urolithin A Protects Chondrocytes From Mechanical Overloading-Induced Injuries.Frontiers in pharmacology · 2021Article
- Role of mitochondria in mediating chondrocyte response to mechanical stimuli.Life sciences · 2020Review
- The role of SIRT3-mediated mitochondrial homeostasis in osteoarthritis.Cellular and molecular life sciences : CMLS · 2020Review
- Mitoprotective therapy prevents rapid, strain-dependent mitochondrial dysfunction after articular cartilage injury.Journal of orthopaedic research : official publication of the Orthopaedic Research Society · 2020Article
- Physiological dynamic compression regulates central energy metabolism in primary human chondrocytes.Biomechanics and modeling in mechanobiology · 2019Article
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Authors and funding
7 authors.
Funding
Abstract
Mechanical loading is essential for articular cartilage homeostasis and plays a central role in the cartilage pathology, yet the mechanotransduction processes that underlie these effects remain unclear. Previously, we showed that lethal amounts of reactive oxygen species (ROS) were liberated from the mitochondria in response to mechanical insult and that chondrocyte deformation may be a source of ROS. To this end, we hypothesized that mechanically induced mitochondrial ROS is related to the magnitude of cartilage deformation. To test this, we measured axial tissue strains in cartilage explants subjected to semi-confined compressive stresses of 0, 0.05, 0.1, 0.25, 0.5, or 1.0 MPa. The presence of ROS was then determined by confocal imaging with dihydroethidium, an oxidant sensitive fluorescent probe. Our results indicated that ROS levels increased linearly relative to the magnitude of axial strains (r(2) = 0.87, p < 0.05), and significant cell death was observed at strains >40%. By contrast, hydrostatic stress, which causes minimal tissue strain, had no significant effect. Cell-permeable superoxide dismutase mimetic Mn(III)tetrakis (1-methyl-4-pyridyl) porphyrin pentachloride significantly decreased ROS levels at 0.5 and 0.25 MPa. Electron transport chain inhibitor, rotenone, and cytoskeletal inhibitor, cytochalasin B, significantly decreased ROS levels at 0.25 MPa. Our findings strongly suggest that ROS and mitochondrial oxidants contribute to cartilage mechanobiology.
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