ArticleScientific reports2022
Regulatory network-based model to simulate the biochemical regulation of chondrocytes in healthy and osteoarthritic environments.
Article in Scientific reports, 2022. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 12 papers.
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Who cites it
12 citing papers in PubMed, 20 citations in OpenAlex.
- A multiscale modeling approach to study the role of mechanics and inflammation in the pathophysiology of articular cartilage.Computers in biology and medicine · 2026Article
- A novel integrative multi-scale framework of inflammation and mechanical loading in knee osteoarthritis.Biomechanics and modeling in mechanobiology · 2026Article
- Exploration of acetylation-related biomarkers in osteoarthritis through bioinformatics analysis.PloS one · 2026Article
- Next-generation osteoarthritis models: integrating biological, computational, and engineering approaches.Stem cell research & therapy · 2025Review
- TNF induces catabolism in human cartilaginous endplate cells in 3D agarose culture under dynamic compression.Scientific reports · 2025Article
- The Effect of Nerve Growth Factor on Cartilage Fibrosis and Hypertrophy duringInternational journal of stem cells · 2025Article
- Nucleus pulposus cell network modelling in the intervertebral disc.NPJ systems biology and applications · 2025Article
- Article
- Towards predicting implant-induced fibrosis: A standardized network model of macrophage-fibroblast interactions.Computational and structural biotechnology journal · 2025Article
- Bioactive Compounds in Osteoarthritis: Molecular Mechanisms and Therapeutic Roles.International journal of molecular sciences · 2024Review
- Network-based modelling of mechano-inflammatory chondrocyte regulation in early osteoarthritis.Frontiers in bioengineering and biotechnology · 2023Article
- The effect of allyl isothiocyanate on chondrocyte phenotype is matrix stiffness-dependent: Possible involvement of TRPA1 activation.Frontiers in molecular biosciences · 2023Article
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Authors and funding
9 authors at 3 institutions in 2 countries.
Funding
No grant is acknowledged in the PubMed record.
Abstract
In osteoarthritis (OA), chondrocyte metabolism dysregulation increases relative catabolic activity, which leads to cartilage degradation. To enable the semiquantitative interpretation of the intricate mechanisms of OA progression, we propose a network-based model at the chondrocyte level that incorporates the complex ways in which inflammatory factors affect structural protein and protease expression and nociceptive signals. Understanding such interactions will leverage the identification of new potential therapeutic targets that could improve current pharmacological treatments. Our computational model arises from a combination of knowledge-based and data-driven approaches that includes in-depth analyses of evidence reported in the specialized literature and targeted network enrichment. We achieved a mechanistic network of molecular interactions that represent both biosynthetic, inflammatory and degradative chondrocyte activity. The network is calibrated against experimental data through a genetic algorithm, and 81% of the responses tested have a normalized root squared error lower than 0.15. The model captures chondrocyte-reported behaviors with 95% accuracy, and it correctly predicts the main outcomes of OA treatment based on blood-derived biologics. The proposed methodology allows us to model an optimal regulatory network that controls chondrocyte metabolism based on measurable soluble molecules. Further research should target the incorporation of mechanical signals.
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