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破骨细胞、巨噬细胞与骨吸收的分子机制

Osteoclasts, macrophages, and the molecular mechanisms of bone resorption.

作者信息

Teitelbaum S L, Tondravi M M, Ross F P

机构信息

Department of Pathology, Washington University School of Medicine, St. Louis, Missouri 63110, USA.

出版信息

J Leukoc Biol. 1997 Apr;61(4):381-8. doi: 10.1002/jlb.61.4.381.

DOI:10.1002/jlb.61.4.381
PMID:9103223
Abstract

The osteoclast is a physiological polykaryon and the major if not exclusive resorptive cell of bone. It participates in bone remodeling, repair, and growth and mobilization of mineral to meet homeostatic demands. Most importantly, osteoporosis, a disease endemic in Western society and Asia, is always a reflection of enhanced osteoclastic activity relative to bone formation by osteoblasts. In fact, all forms of anti-osteoporosis therapy proven successful involve inhibition of osteoclastic bone resorption. Bone resorption is regulated either by altering recruitment of osteoclast precursors into fully differentiated resorptive polykaryons or modulating the rate at which mature osteoclasts degrade bone. With this in mind, our laboratory has focused on the molecular mechanisms of osteoclast differentiation and the means by which the cell degrades bone matrix.

摘要

破骨细胞是一种生理性多核细胞,是骨组织主要的(如果不是唯一的)吸收细胞。它参与骨重塑、修复以及矿物质的生长和动员,以满足体内稳态需求。最重要的是,骨质疏松症在西方社会和亚洲都是一种常见疾病,它始终反映出破骨细胞活性相对于成骨细胞骨形成活性增强。事实上,所有已被证明成功的抗骨质疏松治疗方法都涉及抑制破骨细胞的骨吸收。骨吸收的调节方式要么是改变破骨细胞前体募集到完全分化的吸收性多核细胞的过程,要么是调节成熟破骨细胞降解骨的速率。基于此,我们实验室专注于破骨细胞分化的分子机制以及该细胞降解骨基质的方式。

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