Unraveling the role of FoxOs in bone--insights from mouse models.
Unraveling the role of FoxOs in bone--insights from mouse models.
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DOI：
10.1016/j.bone.2011.05.023
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发表时间：
2011-09
期刊：
影响因子：
4.1
通讯作者：
Almeida, Maria
中科院分区：
文献类型：
--
作者：
Almeida, Maria
FoxO转录因子家族在新陈代谢、分化、增殖、细胞凋亡和应激保护等多种生理过程中发挥重要作用。FOXO活性受到生长因子和胰岛素信号通路的抑制，而受到营养耗竭和过多的ROS诱导的翻译后修饰的刺激。最近的研究揭示了FOXO在骨骼动态平衡中的重要作用。在成骨细胞系的细胞中，Foxos通过激活特定的基因程序以及与其他转录因子和辅助因子如β-catenin、ATF-4和Runx2相互作用来调节氧化还原平衡、蛋白质合成和分化。FOXO的激活也通过细胞自主和间接机制来减弱破骨细胞的形成。在这篇综述中，我讨论了FoxO在成骨细胞前体、成骨细胞和破骨细胞中的特定作用的理解的最新进展，以及FoxO激活对年龄相关性骨骼退化的影响。
The FoxO subfamily of forkhead transcription factors plays a critical role in a variety of physiological processes including metabolism, differentiation, proliferation, apoptosis and protection from stress. FoxO activity is inhibited by growth factors and the insulin signaling pathways and stimulated by nutrient depletion and a plethora of reactive oxygen species (ROS)-induced post-translational modifications. Recent studies have uncovered a fundamental role for FoxOs in skeletal homeostasis. In cells of the osteoblast lineage, FoxOs modulate redox balance, protein synthesis, and differentiation through the activation of specific gene programs and interaction with other transcription factors and co-factors such as β-catenin, ATF-4, and Runx2. FoxO activation also attenuates osteoclastogenesis through both cell autonomous and indirect mechanisms. In this review I discuss recent advances in the understanding of FoxO specific actions in osteoblast progenitors, osteoblasts, and osteoclast, as well as the implications of FoxO activation for age-related skeletal involution.
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