RANKL/RANK/OPG信号通路对骨代谢和血管钙化作用机制的研究现状  

Research progress of the RANKL/RANK/OPG signaling pathway in the mechanisms of bone metabolism and vascular calcification

作　　者：王江东 沈洲姬 徐鹏杰[1] 王依娜 诸医蒙 胡雨韵 WANG Jiangdong;SHEN Zhouji;XU Pengjie;WANG Yi’na;ZHU Yimeng;HU Yuyun(Lihuili Hospital Affiliated to Ningbo University,Ningbo 315040,China)

机构地区：[1]宁波大学附属李惠利医院,宁波315040

出　　处：《生命的化学》2024年第3期448-455,共8页Chemistry of Life

基　　金：浙江省医药卫生科技计划项目(2022KY1087)。

摘　　要：核因子-κB受体活化因子配体(receptor activator of nuclear factor-kappa B ligand,RANKL)/核因子-κB受体活化因子(receptor activator of nuclear factor kappa B,RANK)/骨保护素(osteoprotegerin,OPG)信号通路是调节骨代谢过程中破骨细胞功能的重要通路。OPG能够与RANKL结合并阻止其与RANK结合,抑制破骨细胞生成从而抑制骨吸收,增加骨密度,改善骨质疏松。其中,RANKL/OPG的比值是骨吸收和骨形成平衡的关键。目前血管钙化已不再被看作是单纯的钙磷的被动沉积,而是由血管平滑肌细胞和内皮细胞主动参与的一种与骨形成相似的病理生理过程。在这个过程中,RANKL/RANK/OPG信号通路也起到重要作用。本文就RANKL/RANK/OPG信号通路在骨代谢和血管钙化中的作用机制进行了综述。The signaling pathway involving the receptor activator of nuclear factor-kappa B ligand(RANKL),receptor activator of nuclear factor-kappa B(RANK),and osteoprotegerin(OPG)plays a crucial role in regulating osteoclast function during bone metabolism.OPG effectively inhibits osteoclast formation,suppresses bone resorption,increases bone density,and improves osteoporosis by binding with RANKL and preventing its interaction with RANK.The balance between bone resorption and bone formation is critically influenced by the ratio of RANKL to OPG.Moreover,vascular calcification is now understood as an active pathological process,similar to bone formation,involving vascular smooth muscle cells and endothelial cells,rather than a passive deposition of calcium and phosphate.In this process,the RANKL/RANK/OPG signaling pathway also plays a significant role.Therefore,this paper comprehensively reviews the mechanisms underlying the functioning of the RANKL/RANK/OPG signaling pathway in bone metabolism and vascular calcification.

关 键 词：核因子-κB受体活化因子 核因子-ΚB受体活化因子配体 骨保护素 骨代谢 血管钙化 

分 类 号：R580[医药卫生—内分泌] R54[医药卫生—内科学]