文献类型：期刊文献

中文题名：从OPG/RANK/RANKL信号转导系统探讨老年性骨质疏松的发病机制

英文题名：Exploring the pathogenesis of senile osteoporosis through the OPG/RANK/RANKL signal transduction system

作者：王凯[1];宋敏[1,2];文皓楠[1];海云翔[1];巩彦龙[1]

第一作者：王凯

机构：[1]甘肃中医药大学,甘肃兰州730000;[2]甘肃中医药大学附属医院,甘肃兰州730020

第一机构：甘肃中医药大学

年份：2020

卷号：26

期号：6

起止页码：910

中文期刊名：中国骨质疏松杂志

外文期刊名：Chinese Journal of Osteoporosis

收录：CSTPCD;;北大核心:【北大核心2017】；CSCD:【CSCD2019_2020】；

基金：甘肃省自然科学基金计划(1506RJZA048);甘肃省中医药防治慢性疾病重点实验室开放基金项目(GSMBKY-2015-07);甘肃省中医药管理局科研课题(GZK-2016-17);研究生创新基金(CX2019-03)。

语种：中文

中文关键词：老年性骨质疏松症;信号通路;发病机制

外文关键词：senile osteoporosis;signaling pathways;pathogenesis

摘要：骨质疏松症属于骨科临床常见的慢性、增龄性疾患,随着全球老龄化的加剧,老年人已成为骨质疏松症的高发人群,后期并发脊柱、四肢及骨盆等重要部位的疏松性骨折是致残、致死的主要原因,严重威胁老年群体的身心健康。在我国,老年性骨质疏松症及其并发症防治方面的医疗投入逐年增长,使得社会经济负担越发繁重。近年来随着研究技术与水平的不断提升,在骨分子生物学领域有了不少突破,发现一些细胞因子和信号通路与骨质疏松症的发生、发展密切相关,其中OPG/RANK/RANKL信号转导系统也在骨代谢中起着关键的调控作用。笔者针对老年性骨质疏松症的发病特点,围绕OPG/RANK/RANKL信号通路在该病发生中的作用机制展开综述,以期拓宽老年性骨质疏松症的防治思路。
Osteoporosis is a chronic,age-related disease in clinical orthopedics.With the increase of global aging,the elderly has become a high-risk population of osteoporosis.The main cause of death and disability of this disease is the fractures of the spine,limbs,and pelvis at the later stage.Osteoporosis seriously threatens the psychological and physical health of the elderly.In China,the medical investment in senile osteoporosis and its complications has increased year by year,which has increased the burden of social economy.In recent years,there have been many significant advances in the field of bone molecular biology with the advancement of research techniques and levels.It has found that cytokines and signaling pathways are closely related to the development of osteoporosis and the development of the disease,among which OPG/RANK/RANKL signal transduction system plays a key regulatory role in bone metabolism.This paper reviews the mechanism of action of OPG/RANK/RANKL signaling pathways in the development of the disease to broaden the thought of prevention and treatment of senile osteoporosis.