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核因子κB受体活化因子配体/核因子κB受体活化因子/骨保护素通路

The RANKL/RANK/OPG pathway.

作者信息

Boyce Brendan F, Xing Lianping

机构信息

Department of Pathology and Laboratory Medicine, University of Rochester Medical Center, 601 Elmwood Avenue, Box 626, Rochester, NY 14642, USA.

出版信息

Curr Osteoporos Rep. 2007 Sep;5(3):98-104. doi: 10.1007/s11914-007-0024-y.

Abstract

Understanding of osteoclast formation and activation has advanced considerably since the discovery of the RANKL/RANK/OPG system in the mid 1990s. Osteoblasts and stromal stem cells express receptor activator of NF-jB ligand (RANKL), which binds to its receptor, RANK, on the surface of osteoclasts and their precursors. This regulates the differentiation of precursors into multinucleated osteoclasts and osteoclast activation and survival both normally and in most pathologic conditions associated with increased bone resorption. Osteoprotegerin (OPG) is secreted by osteoblasts and osteogenic stromal stem cells and protects the skeleton from excessive bone resorption by binding to RANKL and preventing it from interacting with RANK. The RANKL/OPG ratio in bone marrow is thus an important determinant of bone mass in normal and disease states. RANKL/RANK signaling also regulates lymph node formation and mammary gland lactational hyperplasia in mice, and OPG protects large arteries of mice from medial calcification. This article reviews the roles of the RANKL/RANK/OPG system in bone and other tissues.

摘要

自20世纪90年代中期发现RANKL/RANK/OPG系统以来,对破骨细胞形成和激活的理解有了很大进展。成骨细胞和基质干细胞表达核因子κB受体激活剂配体(RANKL),它与其受体RANK结合,RANK位于破骨细胞及其前体细胞表面。这一过程在正常情况下以及在大多数与骨吸收增加相关的病理状况下,都调节着前体细胞向多核破骨细胞的分化以及破骨细胞的激活和存活。骨保护素(OPG)由成骨细胞和成骨基质干细胞分泌,通过与RANKL结合并阻止其与RANK相互作用,从而保护骨骼免受过度的骨吸收。因此,骨髓中的RANKL/OPG比值是正常和疾病状态下骨量的重要决定因素。RANKL/RANK信号传导还调节小鼠的淋巴结形成和乳腺泌乳期增生,并且OPG保护小鼠的大动脉免受中层钙化。本文综述了RANKL/RANK/OPG系统在骨骼和其他组织中的作用。

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