ArticleBritish journal of pharmacology2014
A formyl peptide receptor agonist suppresses inflammation and bone damage in arthritis.
Article in British journal of pharmacology, 2014. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 40 papers, 1 of them a synthesis that pooled it.
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Who cites it
40 citing papers in PubMed, 1 synthesis or guideline pooled it, 70 citations in OpenAlex.
- Recognition of Immune Response for the Early Diagnosis and Treatment of Osteoarthritis.Journal of immunology research · 2015Pooled it
- CREM Marks TCR-Driven T-Cell Activation and Associates with Favorable Prognosis in Papillary Thyroid Carcinoma: A Single-Cell and Bulk Transcriptomic Study.International journal of molecular sciences · 2026Article
- Catalpol mitigates rheumatoid arthritis by targeting neutrophil extracellular trap release.Frontiers in immunology · 2026Article
- Formyl peptide receptor 2: a potential therapeutic target for inflammation-related diseases.Pharmacological reports : PR · 2025Review
- Article
- Single-cell multi-omics identify novel regulators required for osteoclastogenesis during aging.iScience · 2024Article
- Formyl peptide receptors in bone research.Connective tissue research · 2023Review
- Promiscuous Receptors and Neuroinflammation: The Formyl Peptide Class.Life (Basel, Switzerland) · 2022Review
- Formylpeptide receptor 2: Nomenclature, structure, signalling and translational perspectives: IUPHAR review 35.British journal of pharmacology · 2022Review
- Pyridazinones and Structurally Related Derivatives with Anti-Inflammatory Activity.Molecules (Basel, Switzerland) · 2022Article
- Discovery of Heteroaryl Urea Isosteres for Formyl Peptide Receptor 2 Agonists.ACS medicinal chemistry letters · 2022Article
- Annexin-A1: The culprit or the solution?Immunology · 2022Review
- Interplay between Inflammation and Pathological Bone Resorption: Insights into Recent Mechanisms and Pathways in Related Diseases for Future Perspectives.International journal of molecular sciences · 2022Review
- Cytokine-primed umbilical cord mesenchymal stem cells enhanced therapeutic effects of extracellular vesicles on osteoarthritic chondrocytes.Frontiers in immunology · 2022Article
- Pyridinone Derivatives as Interesting Formyl Peptide Receptor (FPR) Agonists for the Treatment of Rheumatoid Arthritis.Molecules (Basel, Switzerland) · 2021Article
- Annexin A1 attenuates cardiac diastolic dysfunction in mice with inflammatory arthritis.Proceedings of the National Academy of Sciences of the United States of America · 2021Article
- Activation of formyl peptide receptor 1 elicits therapeutic effects against collagen-induced arthritis.Journal of cellular and molecular medicine · 2021Article
- Microbiota Signals during the Neonatal Period Forge Life-Long Immune Responses.International journal of molecular sciences · 2021Review
- Review
- Signalling and putative therapeutic molecules on the regulation of synoviocyte signalling in rheumatoid arthritis.Bone & joint research · 2021Article
Corrections and comments
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Authors and funding
10 authors at 3 institutions in 2 countries.
Funding
No grant is acknowledged in the PubMed record.
Abstract
background and purposeAnnexin A1 (AnxA1) is an endogenous anti-inflammatory protein and agonist of the formyl peptide receptor 2 (FPR2). However, the potential for therapeutic FPR ligands to modify immune-mediated disease has been little explored. We investigated the effects of a synthetic FPR agonist on joint disease in the K/BxN model of rheumatoid arthritis (RA) and RA fibroblast-like synoviocytes (FLS). EXPERIMENTAL APPROACH: Arthritis was induced by injection of K/BxN serum at day 0 and 2 in wild-type (WT) or AnxA1(-/-) mice and clinical and histopathological manifestations measured 8-11 days later. WT mice were given the FPR agonist compound 43 (Cpd43) (6 or 30 mg·kg(-1) i.p.) for 4 days. Effects of AnxA1 and Cpd43 on RANKL-induced osteoclastogenesis were assessed in RAW 264.7 cells and human RA FLS and macrophages. KEY
resultsTreatment with Cpd43 before or after the onset of arthritis reduced clinical disease severity and attenuated synovial TNF-α and osteoclast-associated gene expression. Deletion of AnxA1 in mice exacerbated arthritis severity in the K/BxN model. In vitro, Cpd43 suppressed osteoclastogenesis and NFAT activity elicited by RANKL, and inhibited IL-6 secretion by mouse macrophages. In human RA joint-derived FLS and monocyte-derived macrophages, Cpd43 treatment inhibited IL-6 release, while blocking FPR2 or silencing AnxA1 increased this release. CONCLUSIONS AND IMPLICATIONS: The FPR agonist Cpd43 reduced osteoclastogenesis and inflammation in a mouse model of RA and exhibited anti-inflammatory effects in relevant human cells. These data suggest that FPR ligands may represent novel therapeutic agents capable of ameliorating inflammation and bone damage in RA.
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