ArticleOsteoarthritis and cartilage2018
Identification of transcription factors responsible for dysregulated networks in human osteoarthritis cartilage by global gene expression analysis.
Article in Osteoarthritis and cartilage, 2018. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 177 papers.
What it found
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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
177 citing papers in PubMed, 262 citations in OpenAlex.
- Immunity-and-matrix-regulatory cells promote hyaline-like cartilage repair in osteoarthritis.Bioactive materials · 2026Article
- The gene-regulatory evolution of the human skeleton.Nature · 2026Article
- USP25 stabilises GLI1 through K48-linked deubiquitination within a reciprocal regulatory circuit in osteoarthritis models.Clinical and translational medicine · 2026Article
- Network Pharmacology Identifies IKBKB as the Primary Target of Sinomenine in Osteoarthritis, with Accuracy Benchmarking and Orthogonal Validation.Biomedicines · 2026Article
- Integrated Toxicogenomic Analysis Reveals Potential Molecular Signatures Associated with Cadmium-Related Osteoarthritis.Biological trace element research · 2026Article
- Cysteine metabolism dysregulation promotes ferroptosis in osteoarthritis: Insights from multi-species bioinformatics and experimental validation.Journal of orthopaedic translation · 2026Article
- CD5L is a potential negative regulator of chondrocyte apoptosis in osteoarthritis.Osteoarthritis and cartilage open · 2026Article
- Network Model to Predict Age-Related Transcriptional Reprogramming.Aging cell · 2026Article
- Author's reply to the Letters regarding "Cysteine metabolism dysregulation promotes ferroptosis in osteoarthritis: Insights from multi-species bioinformatics and experimental validation".Journal of orthopaedic translation · 2026Article
- Article
- Targeting Osteoporosis-Osteoarthritis Comorbidity: Multi-Omics Identification of SON and Exploration of Therapeutic Agents.International journal of molecular sciences · 2026Article
- YTHDF2-driven degradation of BARX2 mRNA accelerates osteoarthritis progression by enhancing the TOP2A/WNT/β-Catenin axis.Communications biology · 2026Article
- SOX9 represses the human galectin-3 promoter in SW1353 cells: potential implications for osteoarthritis.Scientific reports · 2026Article
- NsPEFs-enriched ADSCs-EVs alleviate osteoarthritis via RSPO3-mediated dual pro-chondrogenic and pro-M2 macrophage properties.Bioactive materials · 2026Article
- γδ T cell-stromal networks modulate matrix composition and vascularity in foreign body response.Nature communications · 2026Article
- Integrated mapping of human meniscus and cartilage eQTLs reveals shared and distinct osteoarthritis genetic drivers.medRxiv : the preprint server for health sciences · 2026Article
- LMO7-mediated ubiquitination of SIRT3 promotes osteoarthritis progression: an investigation using machine learning and molecular dynamics simulations.BMC biology · 2026Article
- Association of single nucleotide polymorphisms in FILIP1-SENP6 and FTO with temporomandibular joint osteoarthritis: clinical and in silico study.Scientific reports · 2026Article
- Computational translation of mouse models of osteoarthritis predicts human disease.Osteoarthritis and cartilage · 2026Article
- HIF-1α and BMAL1 in bone regeneration: crosstalk between hypoxia response and circadian rhythm.Bone research · 2026Review
117 more citing papers are in PubMed but not listed here.
Corrections and comments
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Authors and funding
10 authors at 3 institutions in 2 countries.
Funding
Abstract
objectiveOsteoarthritis (OA) is the most prevalent joint disease. As disease-modifying therapies are not available, novel therapeutic targets need to be discovered and prioritized for their importance in mediating the abnormal phenotype of cells in OA-affected joints. Here, we generated a genome-wide molecular profile of OA to elucidate regulatory mechanisms of OA pathogenesis and to identify possible therapeutic targets using integrative analysis of mRNA-sequencing data obtained from human knee cartilage.
designRNA-sequencing (RNA-seq) was performed on 18 normal and 20 OA human knee cartilage tissues. RNA-seq datasets were analysed to identify genes, pathways and regulatory networks that were dysregulated in OA.
resultsRNA-seq data analysis revealed 1332 differentially expressed (DE) genes between OA and non-OA samples, including known and novel transcription factors (TFs). Pathway analysis identified 15 significantly perturbed pathways in OA with ECM-related, PI3K-Akt, HIF-1, FoxO and circadian rhythm pathways being the most significantly dysregulated. We selected DE TFs that are enriched for regulating DE genes in OA and prioritized these TFs by creating a cartilage-specific interaction subnetwork. This analysis revealed eight TFs, including JUN, Early growth response (EGR)1, JUND, FOSL2, MYC, KLF4, RELA, and FOS that both target large numbers of dysregulated genes in OA and are themselves suppressed in OA.
conclusionsWe identified a novel subnetwork of dysregulated TFs that represent new mediators of abnormal gene expression and promising therapeutic targets in OA.
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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.