ArticleScientific reports2024
Mode of injury and level of synovitis alter inflammatory chondrocyte gene expression and associated pathways.
Article in Scientific reports, 2024. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 6 papers, 1 of them a synthesis that pooled it.
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Who cites it
6 citing papers in PubMed, 1 synthesis or guideline pooled it.
- A bibliometric analysis of studies related to the nuclear factor kappa B signaling pathway in knee osteoarthritis between 2004 and 2023.Frontiers in medicine · 2025Pooled it
- Novel Biomaterial-Based Synovial Fluid Analysis Reveals Protective microRNA Signatures in a Mouse Model of Acute Synovitis-Driven Osteoarthritis.FASEB journal : official publication of the Federation of American Societies for Experimental Biology · 2026Article
- Therapeutic effects of Tetramethylpyrazine on Cartilage in Rat Model of Post-traumatic Osteoarthritis.Regenerative therapy · 2026Article
- RNF152-mediated, ubiquitin-dependent degradation of HSP27 activates the PI3K/AKT pathway, driving synovial inflammatory cascades in TMJOA.Arthritis research & therapy · 2025Article
- A Compartmentalized Joint-on-chip (JoC) Model to Unravel the Contribution of Cartilage and Synovium to Osteoarthritis Pathogenesis.Advanced science (Weinheim, Baden-Wurttemberg, Germany) · 2025Article
- Clinical and molecular landscape of post-traumatic osteoarthritis.Connective tissue research · 2025Review
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Authors and funding
9 authors.
Funding
Abstract
Although various joint injuries result in post-traumatic osteoarthritis (PTOA), differences in chondrocyte response to specific injuries, such as blunt compression or fracture, are unclear. Furthermore, the role of underlying joint inflammation, or synovitis, is often not considered. We investigated how injury mechanisms and underlying synovitis affect chondrocyte gene expression using osteochondral injury models with synovial co-culture. We hypothesized that the state of synovitis as well as the mechanism of biomechanical cartilage injury differentially alter the gene expression of chondrocytes and that these responses are regulated by the pro-inflammatory cytokine interleukin 1 (IL-1). The mechanism of injury and level of synovial inflammation both significantly regulated chondrocyte gene expression and associated pathways, uncovering distinct characteristics of fracture and compression injury mechanisms. Targeting IL-1 following injury reduced the inflammatory response and could have clinical implications. The results from this study show that crosstalk between biomechanics and inflammation in the context of synovitis and cartilage injury mechanism is an important consideration for PTOA.
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