Musculoskeletal Disease Area, Novartis Institutes for BioMedical Research, CH-4002 Basel, Switzerland.
Trends Endocrinol Metab. 2010 Apr;21(4):237-44. doi: 10.1016/j.tem.2009.12.002. Epub 2010 Jan 13.
Parathyroid hormone (PTH) has bone anabolic activity when administered intermittently, affecting cells of the osteoblastic lineage at various stages, yet much remains to be learned about precisely how PTH promotes osteoblastic bone formation. Recent discoveries revealed that PTH causes transcriptional suppression of the osteocyte marker gene SOST, which encodes the potent secreted bone formation inhibitor, sclerostin. This review addresses whether osteocytes, terminally differentiated cells of the osteoblastic lineage, which are entrapped within the mineralized bone matrix, contribute to PTH-induced bone formation responses via regulation of sclerostin levels, and discusses recent evidence on how the bone anabolic responses elicited by intermittent PTH treatment or by sclerostin inhibition overlap and diverge.
甲状旁腺激素（PTH）在间歇性给药时具有骨合成代谢活性，影响成骨细胞谱系的各种细胞，但关于 PTH 如何促进成骨细胞骨形成仍有许多需要了解。最近的发现表明，PTH 导致成骨细胞标志物基因 SOST 的转录抑制，SOST 编码强效的分泌性骨形成抑制剂，骨硬化蛋白。本综述探讨了成骨细胞（成骨细胞谱系的终末分化细胞）是否通过调节骨硬化蛋白水平来促进 PTH 诱导的骨形成反应，以及讨论了间歇性 PTH 治疗或骨硬化蛋白抑制引起的骨合成代谢反应的重叠和分歧的最新证据。
