RANKL与骨重建  

The Role of RANKL in Bone Remodeling

作　　者：陈秋月[1] 商澎[1] 

机构地区：[1]西北工业大学生命学院,西北工业大学特殊环境生物物理学研究所,空间生物实验模拟技术国防重点学科实验室.西安710072

出　　处：《中国生物化学与分子生物学报》2013年第5期425-429,共5页Chinese Journal of Biochemistry and Molecular Biology

基　　金：国家自然科学基金项目(No.30970689)~~

摘　　要：骨是一种动态更新的组织,它不断进行骨吸收(bone resorption)与骨形成(bone formation)的平衡,这个过程称之为骨重建(bone remodeling).核因子κB受体活化因子配体(receptor activator of nuclear factorκB ligand,RANKL)是骨吸收和骨形成耦联的关键,具有诱导破骨细胞(osteoclast,OC)生成、活化,抑制破骨细胞凋亡的作用.RANKL最初发现于活化的T细胞,但骨重建过程中RANKL主要来源于骨细胞、成骨细胞和骨髓基质细胞.RANKL/核因子κB受体活化因子(receptor activator of nuclear factorκB,RANK)/骨保护素(osteoprotegerin,OPG)信号通路在成骨细胞调控破骨细胞生成的过程中起着重要的调节作用,是维持骨重建平衡的关键.本文就RANKL及其在骨中的分子作用机制作一综述.Bone is a dynamic tissue resulting from coordinated phases of resorption and formation constantly, which is called bone remodeling. Receptor activator of nuclear factor KB ligand （RANKL） plays a pivotal role in the coupled balance between bone resorption and bone formation, and has the abilities to induce osteoclastogenesis, activating osteoclasts and inhibiting osteoclast apoptosis. RANKL is originally found in activated T cells, but the main sources of RANKL in bone remodeling in vivo are osteocytes,osteoblasts and marrow stromal cells. RANKL/RANK/OPG system plays a significant role in the process of osteoblasts controlling osteoclastogenesis, at the meantime, the crux of maintaining the balance of bone remodeling. This paper reviews RANKL and its molecular mechanism of action in bone.

关 键 词：核因子ΚB受体活化因子配体 骨重建 破骨细胞 

分 类 号：Q71[生物学—分子生物学]