ArticleJournal of translational medicine2023
Complement factor H attenuates TNF-α-induced inflammation by upregulating EIF3C in rheumatoid arthritis.
Article in Journal of translational medicine, 2023. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 15 papers.
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Who cites it
15 citing papers in PubMed, 19 citations in OpenAlex.
- Dual Action of Dipyridamole in Experimental Rheumatoid Arthritis: Suppression of Joint Inflammation and Upregulation of Muscle Anabolism via Adenosine and AMPK Pathways.Arthritis & rheumatology (Hoboken, N.J.) · 2026Article
- Deucravacitinib Inhibits Synovial Fibroblast Activation Via TYK2/STAT3 and PI3K/Akt Signaling Pathway.Inflammation · 2026Article
- Parvimonas micra exacerbates periodontitis by infiltrating host cells through TmpC and circumventing lysosomal elimination via AppA.EBioMedicine · 2026Article
- Precision medicine in rheumatoid arthritis: advances and clinical applications of multi-omics biomarkers.Frontiers in immunology · 2026Review
- Astragalosides Promote MH7A Cell Apoptosis by Suppressing WTAP-mediated m6A Methylation of TRAIL-DR4.Combinatorial chemistry & high throughput screening · 2026Article
- Uncovering the Tumorigenic Blueprint of PFOS and PFOA Through Multi-Organ Transcriptomic Analysis of Biomarkers, Mechanisms, and Therapeutic Targets.Current issues in molecular biology · 2025Article
- Integration of Bioinformatics, Serum Pharmacochemistry, and Metabolomics to Reveal the Mechanisms of Danggui Buxue Decoction in Anti-Rheumatoid Arthritis Through Inflammation and NF-κB Signaling Pathway Regulation.Immunity, inflammation and disease · 2025Article
- Analysis of human factor H-related gene and protein expressed in rheumatoid arthritis synovium identifies a novel mechanism promoting dysregulated complement pathway activation.Scientific reports · 2025Article
- Enhancing Tendon Regeneration: Investigating the Impact of Topography on the Secretome of Adipose-Derived Stem Cells.Advanced science (Weinheim, Baden-Wurttemberg, Germany) · 2025Article
- Disease-Associated Signatures Persist in Extracellular Vesicles from Reprogrammed Cells of Osteoarthritis Patients.International journal of molecular sciences · 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
- Hypocomplementemia dynamics during tocilizumab therapy in systemic juvenile idiopathic arthritis: a retrospective longitudinal study.Frontiers in immunology · 2025Article
- Article
- Eukaryotic initiation factors: central factor associating mRNA translational plasticity during neuropathic pain progression.Frontiers in neurology · 2025Review
- Deciphering the Role of LncRNAs in Osteoarthritis: Inflammatory Pathways Unveiled.Journal of inflammation research · 2024Review
Corrections and comments
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Authors and funding
10 authors at 1 institution in 1 country.
Funding
Abstract
objectiveTo explore the role and underlying mechanism of Complement Factor H (CFH) in the peripheral and joint inflammation of RA patients.
methodsThe levels of CFH in the serum and synovial fluid were determined by ELISA. The pyroptosis of monocytes was determined by western blotting and flow cytometry. The inflammation cytokine release was tested by ELISA. The cell migration and invasion ability of fibroblast-like synoviocytes (FLS) were tested by Wound healing Assay and transwell assay, respectively. The potential target of CFH was identified by RNA sequencing.
resultsCFH levels were significantly elevated in the serum and synovial fluid from RA and associated with high sensitivity C-reactive protein (hs-CRP), erythrocyte sedimentation rate (ESR), and disease activity score 28 (DAS28). TNF-α could inhibit CFH expression, and CFH combined with TNF-α significantly decreased cell death, cleaved-caspase 3, gasdermin E N-terminal (GSDME-N), and inflammatory cytokines release (IL-1β and IL-6) of RA-derived monocytes. Stimulated with TNF-α increased CFH levels in RA FLS and CFH inhibits the migration, invasion, and TNF-α-induced production of inflammatory mediators, including proinflammatory cytokines (IL-6, IL-8) as well as matrix metalloproteinases (MMPs, MMP1 and MMP3) of RA FLSs. The RNA-seq results showed that CFH treatment induced upregulation of eukaryotic translation initiation factor 3 (EIF3C) in both RA monocytes and FLS. The migration of RA FLSs was promoted and the expressions of IL-6, IL-8, and MMP-3 were enhanced upon EIF3C knockdown under the stimulation of CFH combined with TNF-α.
conclusionIn conclusion, we have unfolded the anti-inflammatory roles of CFH in the peripheral and joints of RA, which might provide a potential therapeutic target for RA patients.
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