Role of RANKL and RANK in bone loss and arthritis
SCIE
SCOPUS
- Title
- Role of RANKL and RANK in bone loss and arthritis
- Authors
- Jones, DH; Kong, YY; Penninger, JM
- Date Issued
- 2002-11
- Publisher
- BRITISH MED JOURNAL PUBL GROUP
- Abstract
- The tumour necrosis, factor family molecule RANKL (RANKL, TRANCE, ODF) and its receptor RANK are key regulators of bone remodeling an dendritic cell communications, and lymph node formation. Moreover, RANKL and RANK are expressed, in mammary gland epithelial cells,and control the development of a lactating mammary gland during pregnancy and the propagation of mammalian species. Importantly, RANKL and RANK are essential for the development and activation of osteoclasts and bone loss in response to virtually all triggers tested. Therapeutically, inhibition of RANKL function via the decoy receptor osteoprotegerin completely prevents bone loss at inflammed joints and has partially beneficial effects on cartilage destruction in all arthritis models studied. Modulation of these systems provides a unique opportunity to design novel treatments to inhibit bone loss and crippling in arthritis.
- Keywords
- TUMOR-NECROSIS-FACTOR; NF-KAPPA-B; TNF FAMILY MEMBER; OSTEOCLASTOGENESIS-INHIBITORY FACTOR; OSTEOPROTEGERIN MESSENGER-RNA; LYMPH-NODE ORGANOGENESIS; HUMAN OSTEOBLASTIC CELLS; RECEPTOR ACTIVATOR; FACTOR-ALPHA; RHEUMATOID-ARTHRITIS
- URI
- https://oasis.postech.ac.kr/handle/2014.oak/18853
- DOI
- 10.1136/ard.61.suppl_2.ii32
- ISSN
- 0003-4967
- Article Type
- Article
- Citation
- ANNALS OF THE RHEUMATIC DISEASES, vol. 61, page. 32 - 39, 2002-11
- Files in This Item:
- There are no files associated with this item.
Items in DSpace are protected by copyright, with all rights reserved, unless otherwise indicated.