核因子κB受体活化因子配体（RANKL）和核因子κB受体活化因子（RANK）在骨质流失和关节炎中的作用。
Role of RANKL and RANK in bone loss and arthritis.
作者信息
Jones D Holstead, Kong Y-Y, Penninger J M
机构信息
Institute for Molecular Biotechnology of the Austrian Academy of Sciences, Vienna, Austria.
出版信息
Ann Rheum Dis. 2002 Nov;61 Suppl 2(Suppl 2):ii32-9. doi: 10.1136/ard.61.suppl_2.ii32.
Abstract
The tumour necrosis factor family molecule RANKL (RANKL, TRANCE, ODF) and its receptor RANK are key regulators of bone remodelling and regulate T cell/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.
摘要
肿瘤坏死因子家族分子RANKL（RANKL、TRANCE、ODF）及其受体RANK是骨重塑的关键调节因子，调控T细胞/树突状细胞通讯以及淋巴结形成。此外，RANKL和RANK在乳腺上皮细胞中表达，并在孕期控制泌乳乳腺的发育以及哺乳动物物种的繁衍。重要的是，RANKL和RANK对于破骨细胞的发育和激活以及对几乎所有测试诱因产生的骨质流失至关重要。在治疗方面，通过诱饵受体骨保护素抑制RANKL功能可完全防止炎症关节处的骨质流失，并且在所有研究的关节炎模型中对软骨破坏具有部分有益作用。对这些系统进行调节为设计抑制骨质流失和关节炎致残的新型治疗方法提供了独特机会。
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