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Role of RANKL and RANK in bone loss and arthritis

Title
Role of RANKL and RANK in bone loss and arthritis
Authors
Jones, DHKong, YYPenninger, JM공영윤
Date Issued
Jan-2002
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
http://oasis.postech.ac.kr/handle/2014.oak/18853
ISSN
0003-4967
Article Type
PROCEEDINGS PAPER
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