血管紧张素Ⅱ调控骨代谢的研究进展  

Research progress on regulation of angiotensin Ⅱ on bone metabolism

作　　者：刘金鑫[1] 张方怡[1] 张岩[1] 

机构地区：[1]上海理工大学系统生物医学研究中心,上海200093

出　　处：《中国药理学通报》2015年第4期458-461,共4页Chinese Pharmacological Bulletin

基　　金：国家自然科学基金资助项目(No 81202894)

摘　　要：骨组织中存在局部肾素-血管紧张素系统(RAS)。RAS组分及其活性肽血管紧张素Ⅱ(AngⅡ)直接参与调控骨代谢的病理生理进程。成骨细胞和破骨细胞都有AngⅡ的受体表达,这些受体介导了AngⅡ调控骨代谢的作用。该文回顾了经典RAS途径,探讨了组织RAS致局部组织病变的作用,并对RAS活性肽AngⅡ调控成骨细胞的靶基因、胞内信号通路、AngⅡ通过成骨细胞间接调控破骨细胞功能、AngⅡ受体在骨代谢调控中的交互作用进行了重点阐述。The renin-angiotensin system exists locally in bone tissue. The RAS components and the active peptide angiotensinⅡ（ Ang Ⅱ） within RAS are directly involved in the pathophysiological process of regulating bone metabolism. Ang Ⅱ exerts the effects via its receptors expressed in osteoblasts and osteoclasts.This paper reviewed the pathways of classical RAS,explained the tissue RAS-induced tissue injuries,and especially elaborated the regulation of RAS active peptide Ang Ⅱ on target genes and intracellular signaling pathways in osteoblasts,the action of Ang Ⅱon osteoclastic function via acting on osteoblasts,and the interaction of Ang Ⅱ receptors involved in the modulation on bone metabolism.

关 键 词：肾素-血管紧张素系统 血管紧张素Ⅱ 成骨细胞 破骨细胞 骨质疏松症 受体 

分 类 号：R544.1[医药卫生—心血管疾病]