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Nat Med. 2013 Nov;19(11):1513-7. doi: 10.1038/nm.3364. Epub 2013 Oct 27.
2
Function of matrix IGF-1 in coupling bone resorption and formation.基质 IGF-1 在耦联骨吸收和形成中的功能。
J Mol Med (Berl). 2014 Feb;92(2):107-15. doi: 10.1007/s00109-013-1084-3. Epub 2013 Sep 26.
3
Secondary Knee Osteoarthritis due to Neurofibromatosis Type 1 Treated with above the Knee Amputation: A Case Report.1型神经纤维瘤病所致继发性膝骨关节炎行膝上截肢术治疗：1例报告
Case Rep Orthop. 2013;2013:782106. doi: 10.1155/2013/782106. Epub 2013 Jul 7.
4
Role of T cells in the modulation of PTH action: physiological and clinical significance.T 细胞在甲状旁腺激素作用调节中的作用：生理和临床意义。
Endocrine. 2013 Dec;44(3):576-82. doi: 10.1007/s12020-013-9960-8. Epub 2013 Jun 2.
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Hyperactive transforming growth factor-β1 signaling potentiates skeletal defects in a neurofibromatosis type 1 mouse model.过度活跃的转化生长因子-β1 信号增强了神经纤维瘤病 1 型小鼠模型中的骨骼缺陷。
J Bone Miner Res. 2013 Dec;28(12):2476-89. doi: 10.1002/jbmr.1992.
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Inhibition of TGF-β signaling in mesenchymal stem cells of subchondral bone attenuates osteoarthritis.抑制软骨下骨间充质干细胞中的 TGF-β 信号通路可减轻骨关节炎。
Nat Med. 2013 Jun;19(6):704-12. doi: 10.1038/nm.3143. Epub 2013 May 19.
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Disruption of LRP6 in osteoblasts blunts the bone anabolic activity of PTH.破骨细胞中 LRP6 的缺失削弱了 PTH 的骨合成活性。
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E-selectin ligand 1 regulates bone remodeling by limiting bioactive TGF-β in the bone microenvironment.E-选择素配体 1 通过限制骨微环境中的生物活性 TGF-β 来调节骨重塑。
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Thoracic aortic aneurysm in infancy in aneurysms-osteoarthritis syndrome due to a novel SMAD3 mutation: further delineation of the phenotype.婴儿型胸主动脉瘤伴发于骨关节炎-关节强硬综合征的 SMAD3 基因突变：表型的进一步描绘。
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骨髓间充质干细胞与 TGF-β 信号在骨重塑中的作用。

Bone marrow mesenchymal stem cells and TGF-β signaling in bone remodeling.

出版信息

J Clin Invest. 2014 Feb;124(2):466-72. doi: 10.1172/JCI70050. Epub 2014 Feb 3.

DOI:10.1172/JCI70050
PMID:24487640
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC3904610/
Abstract

During bone resorption, abundant factors previously buried in the bone matrix are released into the bone marrow microenvironment, which results in recruitment and differentiation of bone marrow mesenchymal stem cells (MSCs) for subsequent bone formation, temporally and spatially coupling bone remodeling. Parathyroid hormone (PTH) orchestrates the signaling of many pathways that direct MSC fate. The spatiotemporal release and activation of matrix TGF-β during osteoclast bone resorption recruits MSCs to bone-resorptive sites. Dysregulation of TGF-β alters MSC fate, uncoupling bone remodeling and causing skeletal disorders. Modulation of TGF-β or PTH signaling may reestablish coupled bone remodeling and be a potential therapy.

摘要

在骨吸收过程中，大量先前埋藏在骨基质中的因子被释放到骨髓微环境中，这导致骨髓间充质干细胞（MSCs）的募集和分化，以进行随后的骨形成，从而在时间和空间上偶联骨重塑。甲状旁腺激素（PTH）协调许多直接指导 MSC 命运的信号通路的信号。破骨细胞骨吸收过程中基质 TGF-β的时空释放和激活招募 MSCs 到骨吸收部位。TGF-β的失调改变了 MSC 的命运，使骨重塑解偶联，并导致骨骼疾病。TGF-β或 PTH 信号的调节可能重建偶联的骨重塑，并且是一种潜在的治疗方法。