Role of RANKL and RANK in bone loss and arthritis
Role of RANKL and RANK in bone loss and arthritis
复制标题
DOI：
10.1136/ard.61.suppl_2.ii32
复制
发表时间：
2002-11-01
影响因子：
27.4
通讯作者：
Penninger, JM
中科院分区：
文献类型：
--
作者：
Jones, DH;Kong, YY;Penninger, JM
肿瘤坏死因子家族分子RANKL（RANKL、TRANCE、ODF）及其受体RANK是骨重建、树突状细胞通讯和淋巴结形成的关键调节因子。此外，RANKL和RANK在乳腺上皮细胞中表达，并控制妊娠期间泌乳乳腺的发育和哺乳动物物种的繁殖。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的触发物的骨丢失都是必不可少的。在治疗上，通过诱饵受体骨保护素抑制RANKL功能完全防止炎症关节的骨丢失，并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。这些系统的调节提供了一个独特的机会，设计新的治疗，以抑制骨丢失和关节炎致残。
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.