OPG、RANK、RANKL的结构、作用机制和在骨疾病中的作用

被引：21

作者：

田虹 ^{[1
]}

樊瑜波 ^{[2
]}

机构：

[1] 北京理工大学生命科学与技术学院

[2] 北京航空航天大学生物与医学工程学院

来源：

现代生物医学进展 | 2010年 / 10卷 / 20期

关键词：

OPG; RANK; RANKL; 破骨细胞; 成骨细胞;

D O I：

10.13241/j.cnki.pmb.2010.20.038

中图分类号：

R580 [];

学科分类号：

1002 ; 100201 ;

摘要：

破骨细胞和成骨细胞分别介导骨的吸收过程和合成过程,而OPG、RANK、RANKL在调节二者的比例中发挥非常重要的作用。RANKL与RANK结合后可能通过三种途径:JNK途径、NF-κB途径和蛋白激酶B途径参与破骨细胞的分化,促进骨质的吸收;RANKL与OPG结合后能阻断RANKL与RANK的结合,由于缺乏RANKL-RANK产生的转录活化信号,破骨细胞分化成熟发生障碍,骨质的吸收受到抑制。OPG、RANK、RANKL同时也是免疫分子,在淋巴细胞、淋巴器官的分化、发育中起重要的作用,骨疾病与免疫系统之间存在着一定的关系。RANKL/RANK与RANKL/OPG在生物体内保持着一定的比率,如果比率失衡,就会引起各种骨疾病。本篇综述总结了近年来OPG、RANK、RANKL结构、作用的新进展以及它们在骨疾病中的作用。

引用

页码：3963 / 3966

页数：4

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