Connecting Bone and Fat: The Potential Role for Sclerostin.

Current molecular biology reports Pub Date : 2017-06-01 Epub Date: 2017-04-18 DOI:10.1007/s40610-017-0057-7

Heather Fairfield, Clifford J Rosen, Michaela R Reagan

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Abstract

Sclerostin (SOST), a protein secreted from mature osteocytes in response to mechanical unloading and other stimuli, inhibits the osteogenic Wnt/β-catenin pathway in mesenchymal stem cells (MSCs) impeding their ability to differentiate into mineralizing osteoblasts.

Purpose: This review summarizes the crosstalk between adipose tissue and bone. It also reviews the origin, regulation, and role of SOST in osteogenesis and brings attention to an emerging role of this protein in the regulation of adipogenesis.

Recent findings: Bone-derived molecules that drive MSC adipogenesis have not previously been identified, but recent findings suggest that SOST signaling may induce adipogenesis. In vivo SOST acts locally to induce changes in bone and, in vitro, increases adipogenesis in 3T3-L1 preadipocytes.

Summary: SOST is able to induce adipogenesis in certain preadipocytes, however bone-specific studies are needed to determine the effect of local SOST concentrations in healthy and disease models on bone marrow adipose tissue.

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连接骨骼与脂肪：硬骨蛋白的潜在作用

硬骨素（SOST）是成熟骨细胞在机械卸载和其他刺激下分泌的一种蛋白质，它能抑制间充质干细胞（MSCs）的成骨Wnt/β-catenin通路，阻碍其分化为矿化成骨细胞的能力。目的：这篇综述总结了脂肪组织和骨骼之间的相互关系，还回顾了 SOST 在成骨过程中的起源、调节和作用，并提请人们注意这种蛋白质在调节脂肪生成过程中的新作用：最近的研究结果：之前尚未发现驱动间充质干细胞脂肪生成的骨源性分子，但最近的研究结果表明，SOST 信号传导可能诱导脂肪生成。小结：SOST能诱导某些前脂肪细胞的脂肪生成，但要确定健康和疾病模型中局部SOST浓度对骨髓脂肪组织的影响，还需要进行针对骨骼的研究。

本文章由计算机程序翻译，如有差异，请以英文原文为准。

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Current molecular biology reports

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