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| Smad与骨质疏松症 |
| Smad and osteoporosis |
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| DOI：10.3969/j.issn.1006-7108.2017.08.026 |
| 中文关键词: Smad 骨质疏松症 成骨细胞 破骨细胞 |
| 英文关键词:Smad Osteoporosis Osteoblast Osteoclast |
| 基金项目:广东省科技厅资助项目（20160226） |
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| 中文摘要: |
| 骨质疏松症(osteoporosis，OP)是由成骨细胞(osteoblast，OB)负责的骨形成和破骨细胞(osteoclast，OC)负责的骨吸收之间的平衡被打破所致。已有大量研究证实转化生长因子-β(transforming growth factor-β，TGF-β)通路和骨形态发生蛋白(bone morphogenetic proteins， BMPs)通路能调控骨形成与骨吸收的平衡，而Smad 蛋白家族(Smad)直接介导TGF-β通路和BMP通路下游的信号转导，在调节骨代谢过程中扮演重要的角色。本文针对OP，主要从Smad影响OB与OC的作用方面进行综述。 |
| 英文摘要: |
| Osteoporosis is caused by the disruption of the balance between the osteoblasts responsible for bone formation and the osteoclasts responsible for bone resorption. A large number of studies have confirmed that transforming growth factor-β (TGF-β) and bone morphogenetic proteins (BMPs) signaling pathway can regulate the balance of bone formation and bone resorption. Smad directly mediates the signal transduction in the TGF-β and BMP signaling pathway, and therefore plays an important role in the regulation of bone metabolism. In this paper, we reviewed the influence of Smad on osteoblast and osteoclast in osteoporosis. |
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