连接骨骼与脂肪：硬化蛋白的潜在作用
Connecting Bone and Fat: The Potential Role for Sclerostin.
作者信息
Fairfield Heather, Rosen Clifford J, Reagan Michaela R
机构信息
Maine Medical Research Institute, Scarborough, ME, USA.
University of Maine, Orono, ME, USA.
出版信息
Curr Mol Biol Rep. 2017 Jun;3(2):114-121. doi: 10.1007/s40610-017-0057-7. Epub 2017 Apr 18.
UNLABELLED
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. SOST acts locally to induce changes in bone and, 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.
未标注
硬化蛋白（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，它抑制间充质干细胞（MSC）中的成骨Wnt/β-连环蛋白通路，阻碍其分化为矿化成骨细胞的能力。
目的
本综述总结了脂肪组织与骨骼之间的相互作用。还综述了SOST在骨生成中的起源、调控和作用，并关注该蛋白在脂肪生成调控中的新作用。
最新发现
此前尚未鉴定出驱动MSC脂肪生成的骨源性分子，但最近的研究结果表明，SOST信号可能诱导脂肪生成。SOST在局部发挥作用，诱导骨骼变化，并增加3T3-L1前脂肪细胞的脂肪生成。
总结
SOST能够在某些前脂肪细胞中诱导脂肪生成，然而需要进行骨骼特异性研究，以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。
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