RANKL和OPG与血管钙化  

Correlation between RANKL,OPG and vascular calcification

作　　者：李瑞香[1] 孟凡星[1] 

机构地区：[1]河北省承德医学院病理生理学教研室,河北承德067000

出　　处：《临床心血管病杂志》2014年第4期282-285,共4页Journal of Clinical Cardiology

基　　金：河北省教育厅课题项目(No:Z2010110)

摘　　要：血管钙化是一种可调控的病理过程,与骨化过程有许多相似之处。OPG和RANKL是在骨重建过程中具有重要调控作用的细胞因子,对血管钙化也起重要的调节作用。血管组织内的OPG低表达和RANKL高表达可促进血管钙化的发生,而血清OPG水平升高和血清RANKL水平降低常可作为血管钙化发生的标志。另外,RANKL和OPG对血管钙化的调节作用还受炎性因子、激素、基因多态性等的影响。Vascular calcification is a regulated pathological process, and similar with the process of ossifica- tion. RANKL and OPG are the cytokines which play important regulatory role in the courses of bone remodeling. They also have the regulatory effect on vascular calcification. Low expression of OPG and high expression of RANKL can accelerate vascular calcification in vascular tissue. But increased OPG and reduced RANKL often are regarded as the markers of vascular calcification. Moreover, the regulating effects of RANKL and OPG on vascu- lar calcification are influenced by inflammatory factors, hormones, gene polymorphism, and so on.

关 键 词：OPG RANKL 血管钙化 

分 类 号：R543.5[医药卫生—心血管疾病]