关键词: 11beta-hydroxysteroid dehydrogenase type 1 11β-HSD1 ACPA APC BMSC CK1 CamKII Cthrc1 DKK1 Dickkopf-1 Dvl EZH2 FGF FLS Fibroblast-like synoviocytes GSK3β ILGF-1 LEF LPS LRP MAPK MITF MMPs MSCs Osteoblasts PADI4 PAR-2 PDB PDGF PKC Paget's disease of the bone RA RANKL ROK Rheumatoid arthritis Ror2 SDF-1 SFRP Secreted frizzled-related protein T-cell factors T-cell receptor TCFs TCR VCAM-1 VEGF Wnt signaling pathway Zeste homologue 2 adenomatous polyposis coli alpha-Kelch-like ECT2-interacting protein alphaKLEIP anti-citrullinated peptide antibody bone marrow stromal cell calmodulin kinase II casein kinase 1 collagen triple-helix repeat-containing 1 dickkopf-1 disheveled fibroblast growth factor fibroblast-like synoviocytes glycogen synthase kinase 3β hTERT human telomerase reverse transcriptase insulin like growth factor-1 lipopolysaccharide low-density lipoprotein receptor protein lymphoid enhancer binding factors matrix metalloproteinases mesenchymal stem cells miRNA microRNA microphthalmia-associated transcription factor mitogen-activated protein peptidylarginine deiminase-4 platelet derived growth factor protein kinase C proteinase-activated receptor-2 receptor activator of NFκB ligand receptor tyrosine kinase-like orphan receptor 2 rheumatoid arthritis rho kinase secreted frizzled-related protein stromal cell derived factor 1 vascular cell adhesion molecule-1 vascular-endothelial growth factor

Mesh : Arthritis, Rheumatoid / genetics pathology Bone Remodeling / genetics Cartilage / metabolism Humans Inflammation / genetics pathology Synovial Fluid / cytology metabolism Wnt Proteins / genetics metabolism Wnt Signaling Pathway

来  源:   DOI:10.1016/j.cellsig.2013.04.002

Abstract:
Rheumatoid arthritis (RA) is a chronic symmetrical autoimmune disease of unknown etiology that affects primarily the diarthrodial joints. Characteristic features of RA pathogenesis are synovial inflammation and proliferation accompanied by cartilage erosion and bone loss. Fibroblast-like synoviocytes (FLS) display an important role in the pathogenesis of RA. Several lines of evidence show that the Wnt signaling pathway significantly participates in the RA pathogenesis. The Wnt proteins are glycoproteins that bind to the Fz receptors on the cell surface, which leads to several important biological functions, such as cell differentiation, embryonic development, limb development and joint formation. Accumulated evidence has suggested that this signaling pathway plays a key role in the FLS activation, bone resorption and joint destruction during RA development. Greater knowledge of the role of the Wnt signaling pathway in RA could improve understanding of the RA pathogenesis and the differences in RA clinical presentation and prognosis. In this review, new advances of the Wnt signaling pathway in RA pathogenesis are discussed, with special emphasis on its different roles in synovial inflammation and bone remodeling. Further studies are needed to reveal the important role of the members of the Wnt signaling pathway in the RA pathogenesis and treatment.
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