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[骨髓瘤诱导的骨病机制]

[Mechanisms of myeloma-induced bone disease].

作者信息

Abe Masahiro

机构信息

Department of Hematology, Endocrinology and Metabolism, Tokushima University Graduate School, Japan.

出版信息

Clin Calcium. 2016 May;26(5):699-706.

Abstract

Multiple myeloma(MM)develops and expands almost exclusively in the bone marrow, and generates devastating bone destruction. MM cells produce a variety of cytokines to stimulate RANKL-mediated osteoclastogenesis and suppress osteoblastic differentiation from bone marrow stromal cells, leading to extensive bone destruction with rapid loss of bone. Furthermore, osteocyte apoptosis has been demonstrated to be induced in parallel with enhanced osteoclast recruitment and osteoclastogenesis in myeloma bone lesions. Of note, osteocytes physically interact with myeloma cells to skew their signaling pathways and thereby production of mediators responsible for exacerbated bone resorption and suppressed bone formation in myeloma. The role of osteocytes in myeloma-induced bone lesions remains to be further clarified.

摘要

多发性骨髓瘤(MM)几乎仅在骨髓中发生和发展,并导致严重的骨质破坏。MM细胞产生多种细胞因子,以刺激RANKL介导的破骨细胞生成,并抑制骨髓基质细胞向成骨细胞的分化,导致广泛的骨质破坏和骨量迅速流失。此外,在骨髓瘤骨病变中,已证明骨细胞凋亡与破骨细胞募集增加和成骨细胞生成增强同时发生。值得注意的是,骨细胞与骨髓瘤细胞发生物理相互作用,以改变其信号通路,从而产生负责加剧骨髓瘤中骨吸收和抑制骨形成的介质。骨细胞在骨髓瘤诱导的骨病变中的作用仍有待进一步阐明。

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