破骨细胞 RANKL：骨重建调控的新视角。
Osteocyte RANKL: new insights into the control of bone remodeling.
机构信息
Center for Osteoporosis and Metabolic Bone Diseases, University of Arkansas for Medical Sciences, Little Rock, AR 72205, USA.
出版信息
J Bone Miner Res. 2012 Mar;27(3):499-505. doi: 10.1002/jbmr.1547.
Abstract
The idea that osteoblasts, or their progenitors, support osteoclast formation by expressing the cytokine receptor activator of NFkB ligand (RANKL) is a widely held tenet of skeletal biology. Two recent studies provide evidence that osteocytes, and not osteoblasts or their progenitors, are the major source of RANKL driving osteoclast formation in cancellous bone. The goal of this review is to highlight the results of these new studies and discuss their implications for our understanding of bone remodeling.
摘要
成骨细胞或其前体细胞通过表达核因子κB 配体（RANKL）的细胞因子受体激活物来支持破骨细胞形成的观点是骨骼生物学的一个普遍原则。最近的两项研究提供了证据，表明骨细胞而不是成骨细胞或其前体细胞是松质骨中驱动破骨细胞形成的 RANKL 的主要来源。本文的目的是强调这些新研究的结果，并讨论它们对我们理解骨重塑的意义。
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Sclerostin stimulates osteocyte support of osteoclast activity by a RANKL-dependent pathway.骨硬化蛋白通过 RANKL 依赖性途径刺激骨细胞支持破骨细胞活性。
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