ArticleJournal of orthopaedic research : official publication of the Orthopaedic Research Society2014
Inhibition of cell-matrix adhesions prevents cartilage chondrocyte death following impact injury.
Article in Journal of orthopaedic research : official publication of the Orthopaedic Research Society, 2014. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 13 papers.
What it found
Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.
The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
The trial behind it
Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.
Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.
Who cites it
13 citing papers in PubMed, 34 citations in OpenAlex.
- Early intra-articular complement activation in ankle fractures.BioMed research international · 2014Trial
- Targeting mechanotransduction components as therapeutic strategies in osteoarthritis.Molecular biology reports · 2026Review
- Does the cartilage proteome differ between osteoarthritic knees with varus and valgus deformities? Insights from proteomic analysis.Journal of orthopaedics · 2025Article
- Molecular roles in membrane receptor signaling pathways and cascade reactions in chondrocytes: a review.Journal of molecular histology · 2025Review
- Multiscale Strain Transfer in Cartilage.Frontiers in cell and developmental biology · 2022Review
- Mechanical Loading Disrupts Focal Adhesion Kinase Activation in Mandibular Fibrochondrocytes During Murine Temporomandibular Joint Osteoarthritis.Journal of oral and maxillofacial surgery : official journal of the American Association of Oral and Maxillofacial Surgeons · 2021Article
- Deer antler extract potentially facilitates xiphoid cartilage growth and regeneration and prevents inflammatory susceptibility by regulating multiple functional genes.Journal of orthopaedic surgery and research · 2021Article
- Mechanistic Insight Into the Roles of Integrins in Osteoarthritis.Frontiers in cell and developmental biology · 2021Review
- Article
- Oxidized low density lipoprotein facilitates tumor necrosis factor‑α mediated chondrocyte death via autophagy pathway.Molecular medicine reports · 2017Article
- Complementary models reveal cellular responses to contact stresses that contribute to post-traumatic osteoarthritis.Journal of orthopaedic research : official publication of the Orthopaedic Research Society · 2017Article
- Osteoarthritis year in review 2015: mechanics.Osteoarthritis and cartilage · 2016Review
- Integrins and chondrocyte-matrix interactions in articular cartilage.Matrix biology : journal of the International Society for Matrix Biology · 2014Review
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
3 authors at 1 institution in 1 country.
Funding
Abstract
Focal adhesions are transmembrane protein complexes that attach chondrocytes to the pericellular cartilage matrix and in turn, are linked to intracellular organelles via cytoskeleton. We previously found that excessive compression of articular cartilage leads to cytoskeleton-dependent chondrocyte death. Here we tested the hypothesis that this process also requires integrin activation and signaling via focal adhesion kinase (FAK) and Src family kinase (SFK). Osteochondral explants were treated with FAK and SFK inhibitors (FAKi, SFKi, respectively) for 2 h and then subjected to a death-inducing impact load. Chondrocyte viability was assessed by confocal microscopy immediately and at 24 h post-impact. With no treatment immediate post-impact viability was 59%. Treatment with 10 µM SFKi, 10 μM, or 100 µM FAKi improved viability to 80%, 77%, and 82%, respectively (p < 0.05). After 24 h viability declined to 34% in controls, 48% with 10 µM SFKi, 45% with 10 µM FAKi, and 56% with 100 µM FAKi (p < 0.01) treatment. These results confirmed that most of the acute chondrocyte mortality was FAK- and SFK-dependent, which implicates integrin-cytoskeleton interactions in the death signaling pathway. Together with previous findings, these data support the hypothesis that the excessive tissue strains accompanying impact loading induce death via a pathway initiated by strain on cell adhesion receptors.
Indexed as
Identifiers
What OpenQuestion holds
Registered trials
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.