从Wnt/β-catenin和OPG/RANKL/RANK信号通路探讨糖皮质激素诱发骨质疏松症的可能途径  

Discussion of possible pathways of Wnt/β-catenin and OPG/RANKL/RANK in the pathogenesis of glucocorticoid-induced osteoporosis

作　　者：魏秋实[1,2] 邓伟民[1] 陈现红[1] 黄伟毅[1] 谭新[1] 孙伟珊[1] 邵玉[1] 潘志国[1] 

机构地区：[1]广州军区广州总医院康复科,广州510010 [2]广州军区广州总医院博士后科研工作站,广州510010

出　　处：《中国骨质疏松杂志》2013年第6期626-630,共5页Chinese Journal of Osteoporosis

基　　金：总后勤部卫生部课题(10ZYZ115);广东省科技厅-广东省中医药科学院联合科研专项课题(2011B032200005)

摘　　要：糖皮质激素(Glucocorticoid,GC)主要由肾上腺皮质分泌,因其廉价及具有抗炎和免疫抑制作用,常在肾病综合症、类风湿性关节炎、风湿性多肌痛、结肠炎和慢性阻塞性肺疾病等许多疾病中广泛应用。然而,GC有许多影响代谢的副作用,比如胰岛素抵抗、高血压、青光眼、和骨质疏松症(Osteoporosis,OP)。糖皮质激素性骨质疏松症(Glucocorticoid-induced Osteoporosis,GIOP)是在使用GC治疗疾病过程中引起的骨量丢失,以骨量减少,骨微结构破坏,骨强度下降为特征,导致骨脆性增强,易于发生骨折。GIOP已成为影响人类生活质量的主要问题。随着骨分子生物学的不断发展,GIOP发病机制的研究已渗透到组织,细胞和分子改变的过程中。本文将围绕Wnt/β-catenin与OPG/RANKL/RANK信号通路的交联反应在GIOP发病机制中作用进行讨论,为GIOP基础研究提供新思路。Glucoeorticoid （GC） is mainly secreted by adrenal cortex, which is frequently used in the treatment of a variety of diseases, including nephropathy syndrome, rheumatoid arthritis, polymyalgia rheumatica, colonitis, and chronic obstructive pulmonary disease due to its cheap price, strong anti-inflammatory effect, and immunosuppressive effect. However, GC has many metabolic side effects, such as insulin resistance, hypertension, glaucoma, and osteoporosis （OP）. GC-induced osteoporosis （GIOP）, bone mass loss caused during the treatment using GC, is a disease characterized by bone mass decreasing, microstructural changes of bone tissue, bone strength decreasing, and bone friability increasing, thus being prone to bone fractures. GIOP has become a main problem affecting the quality of human life. With the continuous development of bone molecular biology, the researches of GIOP pathogenesis have penetrated into the processes of the tissue, cell, and molecule changes. This article discusses the crosstalk between Wnt/β-catenin and OPG/RANKL/ RANK in the pathogenesis of GIOP, in order to provide new ideas for the basic research of GIOP.

关 键 词：糖皮质激素 骨质疏松症 

分 类 号：R363[医药卫生—病理学]