Signaling Pathways in Osteoclast Differentiation.

Signaling Pathways in Osteoclast Differentiation.
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DOI:
10.4068/cmj.2016.52.1.12
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发表时间:
2016-01
期刊:
Chonnam medical journal
影响因子:
--
通讯作者:
Kim N
Kim N
中科院分区:
其他
文献类型:
--
作者:
Kim JH;Kim N

文献摘要

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破骨细胞是造血起源的多核细胞,负责旧骨基质的降解。破骨细胞的分化和活性受巨噬细胞集落刺激因子(M-CSF)和核因子-κB配体受体激活因子(RANKL)两种必需细胞因子的控制。M-CSF和RANKL结合各自的受体c-Fms和RANK,通过调节微妙的信号系统刺激破骨细胞分化。在这里,我们总结了破骨细胞分化的关键或必要的信号通路,包括M-CSF-c-Fms信号,RANKL-RANK信号和RANK共刺激信号。
Osteoclasts are multinucleated cells of hematopoietic origin that are responsible for the degradation of old bone matrix. Osteoclast differentiation and activity are controlled by two essential cytokines, macrophage colony-stimulating factor (M-CSF) and the receptor activator of nuclear factor-κB ligand (RANKL). M-CSF and RANKL bind to their respective receptors c-Fms and RANK to stimulate osteoclast differentiation through regulation of delicate signaling systems. Here, we summarize the critical or essential signaling pathways for osteoclast differentiation including M-CSF-c-Fms signaling, RANKL-RANK signaling, and costimulatory signaling for RANK.