TGF-β/SMAD signaling regulation of mesenchymal stem cells in adipocyte commitment

被引：140
作者：
Li, Sheng-Nan [1 ]
Wu, Jia-Fa [2 ]
机构：
[1] Henan Polytech Univ, Sch Med, Jiaozuo 454000, Henan, Peoples R China
[2] Henan Univ Sci & Technol, Sch Food & Bioengn, Luoyang, Henan, Peoples R China
来源：
STEM CELL RESEARCH & THERAPY | 2020年 / 11卷 / 01期
基金：
中国国家自然科学基金;
关键词：
TGF-beta/SMAD signaling; Commitment; Mesenchymal stem cells (MSCs); INDUCED BROWN ADIPOCYTES; MORPHOGENETIC PROTEIN 4; BONE-MARROW; ADIPOGENIC DIFFERENTIATION; PRECURSOR CELLS; STROMAL CELLS; IN-VITRO; BETA; MYOSTATIN; GROWTH;
D O I：
10.1186/s13287-020-1552-y
中图分类号：
Q813 [细胞工程];
学科分类号：
摘要：
Adipocytes arising from mesenchymal stem cells (MSCs) requires MSC adipocyte commitment and differentiation of preadipocytes to mature adipocytes. Several signaling and some cytokines affect the adipogenesis of MSCs. This review focuses on the roles of TGF-beta/SMAD signaling in adipocyte commitment of MSCs. BMP4 and BMP7 signaling are sufficient to induce adipocyte lineage determination of MSCs. The roles of BMP2, TGF-beta, and myostatin signaling in this process are unclear. Other TGF-beta/SMAD signaling such as BMP3 and BMP6 signaling have almost no effect on commitment because of limited research available, while GDF11 signaling inhibits adipocyte commitment in human MSCs. In this review, we summarize the available information on TGF-beta/SMAD signaling regulation of MSCs in adipocyte commitment. Deeper study of this commitment mechanism will offer new approaches in treating obesity, diabetes mellitus, and obesity-related metabolism syndrome.
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页数：10
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