Zaidi Mone
The Mount Sinai Bone Program, Department of Medicine, Box 1055, Mount Sinai School of Medicine, New York, New York 10029, USA.
Nat Med. 2007 Jul;13(7):791-801. doi: 10.1038/nm1593.
The use of genetically manipulated mouse models, gene and protein discovery and the cataloguing of genetic mutations have each allowed us to obtain new insights into skeletal morphogenesis and remodeling. These techniques have made it possible to identify molecules that are obligatory for specific cellular functions, and to exploit these molecules for therapeutic purposes. New insights into the pathophysiology of diseases have also enabled us to understand molecular defects in a way that was not possible a decade ago. This review summarizes our current understanding of the carefully orchestrated cross-talk between cells of the bone marrow and between bone cells and the brain through which bone is constantly remodeled during adult life. It also highlights molecular aberrations that cause bone cells to become dysfunctional, as well as therapeutic options and opportunities to counteract skeletal loss.
基因操纵小鼠模型的应用、基因和蛋白质的发现以及基因突变的编目,都使我们对骨骼形态发生和重塑有了新的认识。这些技术使识别特定细胞功能所必需的分子成为可能,并能将这些分子用于治疗目的。对疾病病理生理学的新认识也使我们能够以十年前不可能的方式理解分子缺陷。本综述总结了我们目前对骨髓细胞之间以及骨细胞与脑之间精心编排的相互作用的理解,通过这种相互作用,骨骼在成年期不断重塑。它还强调了导致骨细胞功能失调的分子异常,以及对抗骨骼流失的治疗选择和机会。