ArticleMolecular medicine (Cambridge, Mass.)2023
Receptor tyrosine kinase C-kit promotes a destructive phenotype of FLS in osteoarthritis via intracellular EMT signaling.
Article in Molecular medicine (Cambridge, Mass.), 2023. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 8 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
8 citing papers in PubMed, 9 citations in OpenAlex.
- Identification of Key Osteoarthritis-Associated Genes Based on DNA Methylation.International journal of molecular sciences · 2026Article
- Computational translation of mouse models of osteoarthritis predicts human disease.Osteoarthritis and cartilage · 2026Article
- Synergistic potential of CDH3 in targeting CRC metastasis and enhancing immunotherapy.BMC cancer · 2025Article
- Comprehensive Analysis Reveals the Potential Diagnostic Value of Biomarkers Associated With Aging and Circadian Rhythm in Knee Osteoarthritis.Orthopaedic surgery · 2025Article
- Computational Translation of Mouse Models of Osteoarthritis Predicts Human Disease.bioRxiv : the preprint server for biology · 2025Article
- Integrative Bulk and Single-Cell Transcriptomic Profiling Reveals Oxidative Stress-Related Genes and Potential Therapeutic Targets in Osteoarthritis.Mediators of inflammation · 2025Article
- The Hippo signalling pathway in bone homeostasis: Under the regulation of mechanics and aging.Cell proliferation · 2024Review
- Role of crosstalk between synovial cells and chondrocytes in osteoarthritis (Review).Experimental and therapeutic medicine · 2024Review
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
6 authors at 1 institution in 1 country.
Funding
Abstract
backgroundChronic inflammation, mainly derived from fibroblast-like synoviocytes (FLSs), plays a central role in the pathomechanism of osteoarthritis (OA). Recently, epithelial-mesenchymal transition (EMT) signaling was found to be activated in OA-derived FLSs with a pro-inflammatory phenotype. However, the role of EMT signaling in regulating FLS function and OA-related inflammation remains unknown.
methodsThe synovium of OA patients were evaluated for EMT and inflammation markers. The FLSs with activated EMT signaling were co-cultured with chondrocytes (chond). Gene expression of OA synovial samples were analyzed. The role of receptor tyrosine kinase C-kit was investigated in OA-FLSs and an OA rat model. The downstream pathways driven by C-kit were explored in OA-FLSs.
resultsEMT marker N-cadherin (N-CDH) was upregulated in 40.0% of the OA samples. These N-CDH
conclusionC-kit drives EMT signaling in OA-FLSs and promotes a destructive FLS phenotype, leading to synovial inflammation and cartilage destruction.
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.