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骨生理学中的成骨细胞——迷你综述

Osteoblasts in bone physiology-mini review.

作者信息

Rosenberg Nahum, Rosenberg Orit, Soudry Michael

机构信息

Musculoskeletal Research Laboratory, Division of Orthopedics, Rambam Health Care Campus, and The Rappaport Faculty of Medicine, Technion-Israel Institute of Technology, Haifa, Israel.

出版信息

Rambam Maimonides Med J. 2012 Apr 30;3(2):e0013. doi: 10.5041/RMMJ.10080. Print 2012 Apr.

Abstract

Bone structural integrity and shape are maintained by removal of old matrix by osteoclasts and in-situ synthesis of new bone by osteoblasts. These cells comprise the basic multicellular unit (BMU). Bone mass maintenance is determined by the net anabolic activity of the BMU, when the matrix elaboration of the osteoblasts equals or exceeds the bone resorption by the osteoclasts. The normal function of the BMU causes a continuous remodeling process of the bone, with deposition of bony matrix (osteoid) along the vectors of the generated force by gravity and attached muscle activity. The osteoblasts are derived from mesenchymal stem cells (MSCs). Circulating hormones and locally produced cytokines and growth factors modulate the replication and differentiation of osteoclast and osteoblast progenitors. The appropriate number of the osteoblasts in the BMU is determined by the differentiation of the precursor bone-marrow stem cells into mature osteoblasts, their proliferation with subsequent maturation into metabolically active osteocytes, and osteoblast degradation by apoptosis. Thus, the two crucial points to target when planning to control the osteoblast population are the processes of cell proliferation and apoptosis, which are regulated by cellular hedgehog and Wnt pathways that involve humoral and mechanical stimulations. Osteoblasts regulate both bone matrix synthesis and mineralization directly by their own synthetic activities, and bone resorption indirectly by its paracrinic effects on osteoclasts. The overall synthetic and regulatory activities of osteoblasts govern bone tissue integrity and shape.

摘要

破骨细胞清除旧基质和成骨细胞原位合成新骨来维持骨结构的完整性和形状。这些细胞构成了基本多细胞单位(BMU)。当成骨细胞的基质生成等于或超过破骨细胞的骨吸收时,BMU的净合成代谢活性决定了骨量的维持。BMU的正常功能导致骨的持续重塑过程,骨基质(类骨质)沿着重力和附着肌肉活动产生的力的方向沉积。成骨细胞来源于间充质干细胞(MSC)。循环激素以及局部产生的细胞因子和生长因子调节破骨细胞和成骨细胞祖细胞的复制和分化。BMU中适当数量的成骨细胞取决于前体骨髓干细胞向成熟成骨细胞的分化、它们的增殖以及随后成熟为代谢活跃的骨细胞,以及通过凋亡导致的成骨细胞降解。因此,在计划控制成骨细胞数量时,需要靶向的两个关键点是细胞增殖和凋亡过程,它们由涉及体液和机械刺激的细胞刺猬信号通路和Wnt信号通路调节。成骨细胞通过自身的合成活动直接调节骨基质的合成和矿化,并通过对破骨细胞的旁分泌作用间接调节骨吸收。成骨细胞的整体合成和调节活动决定了骨组织的完整性和形状。

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