ArticlePloS one2014
Genes involved in the osteoarthritis process identified through genome wide expression analysis in articular cartilage; the RAAK study.
Article in PloS one, 2014. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 107 papers, 4 of them syntheses that pooled it.
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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.
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Who cites it
107 citing papers in PubMed, 4 syntheses or guidelines pooled it, 169 citations in OpenAlex.
- Meta-analysis of erosive hand osteoarthritis identifies four common variants that associate with relatively large effect.Annals of the rheumatic diseases · 2023Pooled it
- Allelic expression imbalance in articular cartilage and subchondral bone refined genome-wide association signals in osteoarthritis.Rheumatology (Oxford, England) · 2023Pooled it
- Meta-analysis of Icelandic and UK data sets identifies missense variants in SMO, IL11, COL11A1 and 13 more new loci associated with osteoarthritis.Nature genetics · 2018Pooled it
- Unique gene expression profile in osteoarthritis synovium compared with cartilage: analysis of publicly accessible microarray datasets.Rheumatology international · 2016Pooled it
- Efficacy, Safety, and Tolerability of ONO-4474, an Orally Available Pan-Tropomyosin Receptor Kinase Inhibitor, in Japanese Patients With Moderate to Severe Osteoarthritis of the Knee: A Randomized, Placebo-Controlled, Double-Blind, Parallel-Group Comparative Study.Journal of clinical pharmacology · 2020Trial
- Reversing detrimental effects of OA-related terminal maturation in high-throughput in vitro and biomimetic ex vivo human models.Arthritis research & therapy · 2026Article
- Evaluating therapeutic efficacy of iopanoic acid in a DMM-induced osteoarthritis mouse model and osteochondral lesioned human explants.Osteoarthritis and cartilage open · 2026Article
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- An explainable ensemble machine learning framework for predicting cartilage biomechanical degradation from transcriptomic profiles: toward smart orthopedic device design.Frontiers in bioengineering and biotechnology · 2026Article
- Connections Between Gene Polymorphism and Fetlock and Hock Measurements in Polish Sport Horses.International journal of molecular sciences · 2025Article
- An Organ-on-Chip Platform for Strain-Controlled, Tissue-Specific Compression of Cartilage and Mineralized Osteochondral Interface to Study Mechanical Overloading in Osteoarthritis.Advanced healthcare materials · 2025Article
- Article
- Development of Reliable and High-Throughput Human Biomimetic Cartilage and Bone Models to Explore Senescence and Personalized Osteoarthritis Treatment Options.Journal of orthopaedic research : official publication of the Orthopaedic Research Society · 2025Article
- Pain mediator NGF improves chondrocyte extracellular matrix synthesis via PI3K/AKT pathway.Journal of orthopaedic surgery and research · 2025Article
- Exploring the therapeutic effect of human recombinant IL11 on lesioned OA human osteochondral explants.Arthritis research & therapy · 2025Article
- Response eQTLs, chromatin accessibility, and 3D chromatin structure in chondrocytes provide mechanistic insight into osteoarthritis risk.Cell genomics · 2025Article
- Augmented expression of superoxide dismutase 2 mitigates progression and rupture of experimental abdominal aortic aneurysm.Theranostics · 2025Article
- Article
- Primary cartilage transcriptional signatures reflect cell-type-specific molecular pathways underpinning osteoarthritis.American journal of human genetics · 2024Article
- Response eQTLs, chromatin accessibility, and 3D chromatin structure in chondrocytes provide mechanistic insight into osteoarthritis risk.bioRxiv : the preprint server for biology · 2024Article
47 more citing papers are in PubMed but not listed here.
Corrections and comments
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Authors and funding
12 authors at 2 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
objectiveIdentify gene expression profiles associated with OA processes in articular cartilage and determine pathways changing during the disease process.
methodsGenome wide gene expression was determined in paired samples of OA affected and preserved cartilage of the same joint using microarray analysis for 33 patients of the RAAK study. Results were replicated in independent samples by RT-qPCR and immunohistochemistry. Profiles were analyzed with the online analysis tools DAVID and STRING to identify enrichment for specific pathways and protein-protein interactions.
resultsAmong the 1717 genes that were significantly differently expressed between OA affected and preserved cartilage we found significant enrichment for genes involved in skeletal development (e.g. TNFRSF11B and FRZB). Also several inflammatory genes such as CD55, PTGES and TNFAIP6, previously identified in within-joint analyses as well as in analyses comparing preserved cartilage from OA affected joints versus healthy cartilage were among the top genes. Of note was the high up-regulation of NGF in OA cartilage. RT-qPCR confirmed differential expression for 18 out of 19 genes with expression changes of 2-fold or higher, and immunohistochemistry of selected genes showed a concordant change in protein expression. Most of these changes associated with OA severity (Mankin score) but were independent of joint-site or sex.
conclusionWe provide further insights into the ongoing OA pathophysiological processes in cartilage, in particular into differences in macroscopically intact cartilage compared to OA affected cartilage, which seem relatively consistent and independent of sex or joint. We advocate that development of treatment could benefit by focusing on these similarities in gene expression changes and/or pathways.
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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.