FGFR1 signaling in rheumatoid arthritis: Mechanisms of bone destruction and therapeutic targeting (Review)
Abstract
Rheumatoid arthritis (RA) is an inflammatory, systematic and articular autoimmune disease characterized by progressive cartilage degradation and bone erosion, leading to irreversible joint deformity. Fibroblast growth factor receptor 1 (FGFR1) is a key mediator of RA‑associated bone loss. Within inflamed joints, FGFR1 expression is markedly upregulated in synovial fibroblasts, osteoclasts and chondrocytes. Ligand engagement drives receptor dimerization and kinase activation, activating PI3K/Akt, MAPK and STAT signaling cascades that amplify cytokine release, matrix metalloproteinase expression and osteoclastogenesis. These converging signals promote cartilage degradation and cortical bone erosion, fueling progressive deformity. Targeting FGFR1 markedly attenuates bone loss and disease severity in both murine and humanized models. The present review aimed to summarize the potential of FGFR1 as a tractable therapeutic node for RA bone destruction.
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