ArticleBone research2022
FABP4 secreted by M1-polarized macrophages promotes synovitis and angiogenesis to exacerbate rheumatoid arthritis.
Article in Bone research, 2022. The graph could read no effect estimate from its abstract, so it casts no vote on the map. An erratum has been issued. Cited by 72 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.
The trial behind it
Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.
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Who cites it
72 citing papers in PubMed, 108 citations in OpenAlex.
- Trial
- Immune remodeling and myeloid signature in the bone marrow niche of MYCN-driven neuroblastoma.BJC reports · 2026Article
- The Multifaceted Roles of Macrophages in Rheumatoid Arthritis: From Cytokine Networks to the Discovery of Novel Subsets.International journal of molecular sciences · 2026Review
- Review
- Orally Administered Self-Microemulsifying Celastrol Alleviates Rheumatoid Arthritis by Modulating the Expression of TNF-α.Pharmaceutics · 2026Article
- Metabolic and neuroimmune control of rheumatoid arthritis: therapeutic implications of FXR and α7-nAChR axes.Inflammopharmacology · 2026Review
- Targeting peptidyl-arginine deiminase 4 suppresses SARS-CoV-2 replication and modulates the inflammatory response.iScience · 2026Article
- FABP4 expression in neutrophils as a predictor of sepsis and SI-ARDS based on BALF transcriptome and peripheral blood validation.Chinese medical journal · 2026Article
- Immunometabolic resistors of aging in long-lived golden spiny mice.Science advances · 2026Article
- Association Between Neutrophil Percentage-Albumin Ratio and Biological Aging in Rheumatoid Arthritis in the United States: A Cross-Sectional Study of NHANES.Mediators of inflammation · 2026Article
- FABP4 as an immunometabolic hub in preeclampsia: from maternal-fetal interface to systemic inflammation.Frontiers in immunology · 2026Review
- CD44/POU2F2/BCL9L axis mediates MIF-driven SPP1International journal of biological sciences · 2026Article
- ANXA1-mediated mTOR/FABP4 Inhibition Drives Antifibrotic Macrophage Reprogramming in Lupus Nephritis.International journal of biological sciences · 2026Article
- Regulation of osteoclastogenesis and bone resorption by fatty acid metabolism: mechanisms and therapeutic opportunities.Frontiers in endocrinology · 2026Review
- The potential involvement of FABP4 in rheumatoid arthritis-associated osteoporosis: a comprehensive bioinformatics analysis and experimental validation.Frontiers in immunology · 2026Article
- Inhibition of fatty acid-binding protein 4 alleviates psoriasis-like skin inflammation by modulating macrophage polarization.Frontiers in immunology · 2026Article
- Cross-tissue single-cell atlas reveals Id2 promotes sepsis-induced tissue damage by mediating macrophage metabolic reprogramming via Pkm2.International journal of biological sciences · 2026Article
- Prenatal Exposure to PMEnvironment & health (Washington, D.C.) · 2025Article
- Fatty acid binding protein 4 induces osteogenesis and angiogenesis as pathogenesis of metabolic osteoarthritis.Molecular medicine (Cambridge, Mass.) · 2025Article
- Senescent SPP1Molecular cancer · 2025Article
12 more citing papers are in PubMed but not listed here.
Corrections and comments
- Erratum issued
Authors and funding
12 authors at 3 institutions in 1 country.
Funding
Abstract
Increasing evidence shows that adipokines play a vital role in the development of rheumatoid arthritis (RA). Fatty acid-binding protein 4 (FABP4), a novel adipokine that regulates inflammation and angiogenesis, has been extensively studied in a variety of organs and diseases. However, the effect of FABP4 on RA remains unclear. Here, we found that FABP4 expression was upregulated in synovial M1-polarized macrophages in RA. The increase in FABP4 promoted synovitis, angiogenesis, and cartilage degradation to exacerbate RA progression in vivo and in vitro, whereas BMS309403 (a FABP4 inhibitor) and anagliptin (dipeptidyl peptidase 4 inhibitor) inhibited FABP4 expression in serum and synovial M1-polarized macrophages in mice to alleviate RA progression. Further studies showed that constitutive activation of mammalian target of rapamycin complex 1 (mTORC1) by TSC1 deletion specifically in the myeloid lineage regulated FABP4 expression in macrophages to exacerbate RA progression in mice. In contrast, inhibition of mTORC1 by ras homolog enriched in brain (Rheb1) disruption specifically in the myeloid lineage reduced FABP4 expression in macrophages to attenuate RA development in mice. Our findings established an essential role of FABP4 that is secreted by M1-polarized macrophages in synovitis, angiogenesis, and cartilage degradation in RA. BMS309403 and anagliptin inhibited FABP4 expression in synovial M1-polarized macrophages to alleviate RA development. Hence, FABP4 may represent a potential target for RA therapy.
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Registered trials
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.