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Wnt signaling pathway in rheumatoid arthritis, with special emphasis on the different roles in synovial inflammation and bone remodeling

期刊

CELLULAR SIGNALLING
卷 25, 期 10, 页码 2069-2078

出版社

ELSEVIER SCIENCE INC
DOI: 10.1016/j.cellsig.2013.04.002

关键词

Rheumatoid arthritis; Fibroblast-like synoviocytes; Wnt signaling pathway; Secreted frizzled-related protein; Dickkopf-1; Osteoblasts

资金

  1. National Science Foundation of China [30873081, 81072686]
  2. Provincial Natural Science Research Project of Colleges and Universities of Anhui Province [KJ2013B082]
  3. Research Project of Anhui Science and Technology University [ZRC2013378]

向作者/读者索取更多资源

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 (C) 2013 Elsevier Inc. All rights reserved.

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