ArticleFrontiers in immunology2023
Citrullinated and malondialdehyde-acetaldehyde modified fibrinogen activates macrophages and promotes an aggressive synovial fibroblast phenotype in patients with rheumatoid arthritis.
Article in Frontiers in immunology, 2023. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 18 papers, 1 of them a synthesis that pooled it.
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Who cites it
18 citing papers in PubMed, 1 synthesis or guideline pooled it, 24 citations in OpenAlex.
- Malondialdehyde-acetaldehyde modified macromolecules and resulting autoantibodies in rheumatoid arthritis pathogenesis: a Systematic Literature Review.Frontiers in immunology · 2025Pooled it
- Article
- Analysis of inflammatory immune correlation of the coagulation spectrum, PT, FBG, FDP, D-D in autoimmune diseases.Journal of medical biochemistry · 2026Article
- The Linkage Between Ecotoxins Within Maximum Permissible Concentrations, Oxidative Stress and Antibodies Against Cyclic Citrullinated Peptides in Patients and Persons at Preclinic Stages of Rheumatoid Arthritis.International journal of molecular sciences · 2026Article
- Gut microbiota dysbiosis in rheumatoid arthritis: mechanisms linking intestinal barrier dysfunction to synovial inflammation.Frontiers in immunology · 2026Review
- Shared genetic architecture and potential comorbid mechanisms between rheumatoid arthritis and idiopathic pulmonary fibrosis.Clinical rheumatology · 2026Article
- Epigenetic modifications of immune cells in rheumatoid arthritis.Annals of medicine · 2025Review
- Citrullinated and Malondialdehyde-Acetaldehyde-Modified Fibrinogen Activates Macrophages and Promotes Coronary Endothelial Cell Inflammation.Current issues in molecular biology · 2025Article
- Integrated analysis of single-cell RNA-seq and bulk RNA-seq reveal macrophage subpopulation characteristics and the role of STAT1 in rheumatoid arthritis.Journal of translational medicine · 2025Article
- Pharmacological Inhibition of the PI3K/AKT/mTOR Pathway in Rheumatoid Arthritis Synoviocytes: A Systematic Review and Meta-Analysis (Preclinical).Pharmaceuticals (Basel, Switzerland) · 2025Review
- Tissue macrophages: origin, heterogenity, biological functions, diseases and therapeutic targets.Signal transduction and targeted therapy · 2025Review
- Citrullinated IGF2BP1 promotes rheumatoid synovial aggression via increasing the mRNA stability of SEMA3D.Communications biology · 2025Article
- MAPK/ERK signaling pathway in rheumatoid arthritis: mechanisms and therapeutic potential.PeerJ · 2025Review
- Citrullinated and malondialdehyde-acetaldehyde-modified fibrinogen activates macrophages and promotes profibrotic responses in human lung fibroblasts.American journal of physiology. Lung cellular and molecular physiology · 2025Article
- Lung disease in relation to unique monocyte-macrophage subpopulations induced by combined inhalant endotoxin and collagen-induced arthritis.Frontiers in immunology · 2025Article
- Antibodies to Malondialdehyde-Acetaldehyde Adduct Are Associated With Prevalent and Incident Rheumatoid Arthritis-Associated Interstitial Lung Disease in US Veterans.Arthritis & rheumatology (Hoboken, N.J.) · 2024Article
- Targeting transitioning lung monocytes/macrophages as treatment strategies in lung disease related to environmental exposures.Respiratory research · 2024Article
- Macrophage polarization in rheumatoid arthritis: signaling pathways, metabolic reprogramming, and crosstalk with synovial fibroblasts.Frontiers in immunology · 2024Review
Corrections and comments
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Authors and funding
10 authors at 2 institutions in 1 country.
Funding
Abstract
Objective: Post-translational protein modifications with malondialdehyde-acetaldehyde (MAA) and citrulline (CIT) are implicated in the pathogenesis of rheumatoid arthritis (RA). Although precise mechanisms have not been elucidated, macrophage-fibroblast interactions have been proposed to play a central role in the development and progression of RA. The purpose of our study was to evaluate the downstream effects of macrophage released soluble mediators, following stimulation with fibrinogen (FIB) modified antigens, on human fibroblast-like synoviocytes (HFLS). Methods: PMA-treated U-937 monocytes (Mϕ) and macrophage-differentiated peripheral blood mononuclear cells (MP) were stimulated with FIB, FIB-MAA, FIB-CIT, or FIB-MAA-CIT. HFLS-RA cells were stimulated directly with FIB antigens or with supernatants (SN) from macrophages (Mϕ-SN or MP-SN) stimulated with FIB antigens. Genes associated with an aggressive HFLS phenotype, extracellular matrix proteins, and activated signaling pathways were evaluated. Results: HFLS-RA cells treated with Mϕ-SN Conclusion: Together, these findings support the hypothesis that in response to MAA-modified and/or citrullinated fibrinogen, macrophages release soluble factors including PDGF-BB that induce fibroblast activation and promote an aggressive fibroblast phenotype. These cellular responses were most robust following macrophage activation with dually modified fibrinogen, compared to single modification alone, providing novel insights into the combined role of multiple post-translational protein modifications in the development of RA.
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