Will reducing adipogenesis in bone increase bone mass?:: PPARγ2 as a key target in the treatment of age-related bone loss
Will reducing adipogenesis in bone increase bone mass?:: PPARγ2 as a key target in the treatment of age-related bone loss
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DOI：
10.1358/dnp.2003.16.6.829305
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发表时间：
2003-07-01
影响因子：
--
通讯作者：
Duque, G
中科院分区：
文献类型：
--
作者：
Duque, G
有多种机制可以解释老年骨质疏松症的病理生理学。其中之一是在衰老过程中观察到的骨髓中脂肪生成水平的增加。众所周知，表达配体激活转录因子（称为过氧化物酶体增殖物激活受体γ（2）（PPARγ（2）））的间充质干细胞致力于分化为脂肪细胞。 PPARgamma(2) 激活的调节可能在控制间充质干细胞的成脂分化中发挥作用，从而有助于它们分化为成骨细胞以形成新骨。在这篇综述中，我们描述了 PPAR 孤儿受体家族的特征，重点是 PPARgamma(2)、其结构和功能特征及其作为治疗老年骨质疏松症的治疗靶点的潜力。 (C) 2003 年《Prous Science》。版权所有。
There are several mechanisms that explain the pathophysiology of senile osteoporosis. One of them is the increasing levels of adipogenesis in bone marrow that are seen during the aging process. It is known that mesenchymal stem cells expressing a ligand-activated transcription factor known as peroxisome proliferator-activated receptor gamma(2) (PPARgamma(2)) are committed to differentiate into adipocytes. The regulation of PPARgamma(2) activation may play a role in the control of adipogenic differentiation of mesenchymal stem cells and thus contribute to their differentiation into osteoblasts in order to form new bone. In this review we describe the characteristics of the orphan receptor family of PPARs, with emphasis on PPARgamma(2), its structural and functional characteristics and its potential as a therapeutic target for the treatment of senile osteoporosis. (C) 2003 Prous Science. All rights reserved.