ArticleGenome biology2021
Functional genomics atlas of synovial fibroblasts defining rheumatoid arthritis heritability.
Article in Genome biology, 2021. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 38 papers, 1 of them a synthesis that pooled it.
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38 citing papers in PubMed, 1 synthesis or guideline pooled it, 52 citations in OpenAlex.
- Hypothyroidism and rheumatoid arthritis: a two-sample Mendelian randomization study.Frontiers in endocrinology · 2023Pooled it
- mFABIO: An integrative multi-tissue TWAS fine-mapping approach to prioritize potentially causal genes and tissues underlying binary traits.PLoS genetics · 2026Article
- Deucravacitinib Inhibits Synovial Fibroblast Activation Via TYK2/STAT3 and PI3K/Akt Signaling Pathway.Inflammation · 2026Article
- RA-risk synovium exhibits DNA damage coupled with impaired DNA repair in fibroblasts.RMD open · 2026Article
- Epigenetic alterations in rheumatoid arthritis: multilayer mechanisms and translational opportunities.Frontiers in immunology · 2026Review
- Multidimensional regulatory mechanisms and translational potential of epigenetic networks in the rheumatoid arthritis disease course.Frontiers in immunology · 2026Review
- Article
- Exploration of potential novel drug targets for rheumatoid arthritis by plasma proteome screening.PLoS computational biology · 2025Article
- Unveiling the Therapeutic Potential: Targeting Fibroblast-like Synoviocytes in Rheumatoid Arthritis.Expert reviews in molecular medicine · 2025Review
- The distinct transcriptomic signature of the resolution phase fibroblast-like synoviocytes supports endothelial cell dysfunction.Communications biology · 2025Article
- Pro-Inflammatory Properties of Salivary Gland-Derived Fibroblasts-Implications in Sjögren's Disease.Cells · 2025Article
- Multi-omics analysis in primary T cells elucidates mechanisms behind disease-associated genetic loci.Genome biology · 2025Article
- CDK6-Dependent, CDK4-Independent Synovial Hyperplasia in Arthritic Mice and Tumor Necrosis Factor-α-Induced Proliferation of Synovial Fibroblasts.International journal of molecular sciences · 2025Article
- Senolytic treatment to rescue hallmarks of senescence in lymph node fibroblasts from patients with rheumatoid arthritis: Implications for premature aging and potential therapeutic intervention in early rheumatoid arthritis.Clinical and experimental immunology · 2025Article
- Integrated Metabolomics and Proteomics to Decipher Simiao Pill Improving Lipid Homeostasis through PTGES3-mediated Arachidonic Acid Metabolism in AIA Model.Current pharmaceutical design · 2025Article
- Activation of the Keap1/Nrf2/HO-1 Pathway by "Tianyu" Pairing: Implications for Inflammation and Oxidative Stress in Rheumatoid Arthritis.Endocrine, metabolic & immune disorders drug targets · 2025Article
- Robust estimation of cancer and immune cell-type proportions from bulk tumor ATAC-Seq data.eLife · 2024Article
- The expression of RBPJ and its potential role in rheumatoid arthritis.BMC genomics · 2024Article
- Article
- Characterizing the polygenic overlap and shared loci between rheumatoid arthritis and cardiovascular diseases.BMC medicine · 2024Article
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18 authors at 5 institutions in 3 countries.
Funding
Abstract
backgroundGenome-wide association studies have reported more than 100 risk loci for rheumatoid arthritis (RA). These loci are shown to be enriched in immune cell-specific enhancers, but the analysis so far has excluded stromal cells, such as synovial fibroblasts (FLS), despite their crucial involvement in the pathogenesis of RA. Here we integrate DNA architecture, 3D chromatin interactions, DNA accessibility, and gene expression in FLS, B cells, and T cells with genetic fine mapping of RA loci.
resultsWe identify putative causal variants, enhancers, genes, and cell types for 30-60% of RA loci and demonstrate that FLS account for up to 24% of RA heritability. TNF stimulation of FLS alters the organization of topologically associating domains, chromatin state, and the expression of putative causal genes such as TNFAIP3 and IFNAR1. Several putative causal genes constitute RA-relevant functional networks in FLS with roles in cellular proliferation and activation. Finally, we demonstrate that risk variants can have joint-specific effects on target gene expression in RA FLS, which may contribute to the development of the characteristic pattern of joint involvement in RA.
conclusionOverall, our research provides the first direct evidence for a causal role of FLS in the genetic susceptibility for RA accounting for up to a quarter of RA heritability.
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