MAPK信号通路与骨质疏松关系的研究进展  

Relations between the MAPKs and the osteoporosis

作　　者：张波[1] 耿彬[1] 谭小义[1] 姜金[1] 陈聪[1] Chandan Kumar Jayswal 吴卓[1] 夏亚一[1] 

机构地区：[1]兰州大学第二临床医学院骨科,兰州730000

出　　处：《中国矫形外科杂志》2014年第23期2161-2164,共4页Orthopedic Journal of China

基　　金：国家自然科学基金(编号:81071478);甘肃省自然基金(1107RJZA144)

摘　　要：该综述介绍了MAPK信号通路(ERK1/2、JNK、P38和ERK5)与骨质疏松相关因子的关系,明确了MAPK信号通路参与骨质疏松的发生与发展。通过药物干预RANKL、OPG、1,25(OH)2D3、PTH、BMP、TGF-β、IL-1、IL-6、TNF-α和雌激素等因子而作用于MAPK信号通路,可提高骨质疏松的治疗效果。但IL6和TNF-α调节MAPK信号通路参与骨质疏松发生发展的作用还不清楚。骨质疏松发病机制复杂,多种相关信号通路之间存在交互和交叉的作用,以及ERK5通路在骨质疏松中发挥的作用还有待进一步研究。This review introduces a relatively new signal transduction pathway about Mitogen- activated protein（ MAP）kinase family,including four subfamily members which are extracellular signal- regulated kinases（ ERK1 /2）,c- Jun N-terminal kinases（ JNK1,2,and3）,p38 kinase（ α,β,γ,δ） and big MAP kinase（ BMK or ERK5）,and respectively illustrates MAPK family involved in the development of osteoporosis. Many drugs improving therapeutic effect of osteoporosis may intervene MAPK signal transduction pathway by RANKL,OPG,1,25（ OH） 2D3,PTH,BMP,TGF- β,IL- 1,IL- 6,TNF- α and estrogen. However,the role of IL- 6 and TNF- α for MAPKs involved in development of osteoporosis is not clear. The pathogenesis of osteoporosis exist many interactions of different signal pathways,and the molecular mechanisms regulating osteoporosis by ERK5 have remained to be elucidated.

关 键 词：信号传导通路 MAPK 骨质疏松 

分 类 号：R580[医药卫生—内分泌]