ReviewFrontiers in immunology2026
FGF/FGFR signaling at the immune-stromal interface in autoimmune rheumatic diseases: from tissue remodeling to translational opportunities.
Review in Frontiers in immunology, 2026. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Not yet cited in PubMed.
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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.
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7 authors.
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Abstract
The fibroblast growth factor (FGF)/FGF receptor (FGFR) signaling system regulates tissue repair, angiogenesis, extracellular matrix remodeling, fibrosis, and bone metabolism. Although FGF/FGFR biology has been extensively studied in oncology, development, and fibrotic lung disease, its relevance to systemic autoimmune rheumatic diseases remains scattered across disease-specific and unevenly supported literatures. This narrative, evidence-informed review synthesizes current evidence on FGF/FGFR signaling in rheumatoid arthritis (RA), systemic lupus erythematosus/lupus nephritis (SLE/LN), systemic sclerosis (SSc), spondyloarthritis/psoriatic arthritis (SpA/PsA), and Sjögren's disease. We explicitly distinguish mechanistically supported axes from biomarker-level associations and extrapolated regenerative concepts. In RA, FGF10/FGFR1 and FGF2/FGFR3 have the strongest tissue-level support, linking relapse-prone synovial fibroblast niches, fibroblast-like synoviocyte activation, angiogenesis, and bone erosion. In SLE/LN, FGF23/Klotho is best interpreted as an emerging renal-metabolic and inflammatory biomarker axis rather than a validated therapeutic target, although reported associations with urinary MCP-1/CCL2 suggest testable links to renal chemokine-mediated inflammation. In SSc-ILD, nintedanib demonstrates that FGFR-containing multi-kinase networks are clinically tractable, but the FGFR-specific contribution remains unresolved. In SpA/PsA, FGF2-mediated angiogenesis-osteogenesis coupling and FGF7/FGFR2IIIb signaling provide candidate mechanisms for entheseal remodeling, whereas direct human entheseal validation is still lacking. In Sjögren's disease, FGF7/FGF10/FGFR2b signaling supports a regenerative hypothesis derived mainly from salivary gland developmental biology and organoid studies. We propose an axis-prioritization translational framework that specifies ligand-receptor pairs, patient subgroups, validation tissues, delivery strategies, pharmacodynamic endpoints, and clinical or imaging readouts. This review is not a systematic review or meta-analysis; rather, it provides a structured roadmap for tissue-level validation, longitudinal biomarker studies, and short-course proof-of-mechanism trials before clinical translation.
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