Poole Kenneth E S, Reeve Jonathan
Division of Bone Research, Department of Medicine, Level 5, University of Cambridge, Addenbrooke's Hospital (Box 157), Cambridge CB2 2QQ, UK.
Curr Opin Pharmacol. 2005 Dec;5(6):612-7. doi: 10.1016/j.coph.2005.07.004. Epub 2005 Sep 21.
A key factor in the control of bone remodelling is parathyroid hormone (PTH), the principal regulator of calcium homeostasis. Elevated levels of PTH increase bone turnover, leading to either anabolic or catabolic effects on the skeleton depending upon the pattern and duration of elevation. New evidence indicating that downregulation of an osteocyte signal (sclerostin, the SOST gene product) occurs in response to intermittent PTH has rekindled interest in the key role played by osteocytes and bone-lining cells in co-ordinating surface anabolic activity. Microarray analysis has also delineated many genes and pathways regulated by intermittent and continuous PTH in osteoblasts and whole bones.
控制骨重塑的一个关键因素是甲状旁腺激素(PTH),它是钙稳态的主要调节因子。PTH水平升高会增加骨转换,根据升高的模式和持续时间,对骨骼产生合成代谢或分解代谢作用。新证据表明,骨细胞信号(硬化蛋白,SOST基因产物)的下调是对间歇性PTH的反应,这重新引发了人们对骨细胞和骨衬细胞在协调表面合成代谢活动中所起关键作用的兴趣。微阵列分析还描绘了成骨细胞和全骨中受间歇性和持续性PTH调节的许多基因和途径。