Osteoprotegerin and RANKL regulate bone resorption, density, geometry and strength
Osteoprotegerin and RANKL regulate bone resorption, density, geometry and strength
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DOI：
10.1016/j.coph.2005.06.005
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发表时间：
2005-12-01
影响因子：
4
通讯作者：
Kostenuik, PJ
中科院分区：
文献类型：
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作者：
Kostenuik, PJ
骨保护素（OPG）和核因子-κ B配体受体激活因子（RANKL）是骨吸收的主要调节因子。许多激素、细胞因子和生长因子通过改变RANKL与OPG的比例来介导骨吸收。RANKL和OPG表达在许多骨疾病中也发生改变，这些变化可以反映疾病病因或对疾病的代偿反应。RANKL刺激破骨细胞的形成、功能和存活，而OPG可抑制这些作用。OPG抑制骨吸收并增加松质骨和皮质骨的密度、面积和强度。Denosumab（AMG 162）是一种RANKL的全人源单克隆抗体，具有OPG的药理学属性，但半衰期显著更长，因此给药频率较低。
Osteoprotegerin (OPG) and receptor activator of nuclear factor-kappa B ligand (RANKL) are dominant regulators of bone resorption. Many hormones, cytokines and growth factors mediate bone resorption by altering the ratio of RANKL to OPG. RANKL and OPG expression is also altered in numerous bone diseases, and these changes can reflect disease etiology or compensatory responses to disease. RANKL stimulates osteoclast formation, function and survival, and each of these effects is inhibited by OPG. OPG suppresses bone resorption and increases the density, area and strength of both cancellous and cortical bone. Denosumab (AMG 162), a fully human monoclonal antibody to RANKL, shares the pharmacologic attributes of OPG but has a significantly longer half-life that allows less frequent administration.