Wang Ruo-Yu, Yang Shu-Hua, Xu Wei-Hua
Department of Orthopedics, Union Hospital, Tongji Medical College, Huazhong University of Science and Technology, Wuhan, Hubei 430022, China.
Chin Med J (Engl). 2016 Mar 5;129(5):594-600. doi: 10.4103/0366-6999.176994.
To review the recent developments in the mechanisms of epithelium sodium channels (ENaCs) induced bone formation and regulation.
Studies written in English or Chinese were searched using Medline, PubMed and the index of Chinese-language literature with time restriction from 2005 to 2014. Keywords included ENaC, bone, bone formation, osteonecrosis, estrogen, and osteoporosis. Data from published articles about the structure of ENaC, mechanism of ENaC in bone formation in recent domestic and foreign literature were selected.
Abstract and full text of all studies were required to obtain. Studies those were not accessible and those did not focus on the keywords were excluded.
ENaCs are tripolymer ion channels which are assembled from homologous α, β, and γ subunits. Crystal structure of ENaCs suggests that ENaC has a central ion-channel located in the central symmetry axis of the three subunits. ENaCs are protease sensitive channels whose iron-channel activity is regulated by the proteolytic reaction. Channel opening probability of ENaCs is regulated by proteinases, mechanical force, and shear stress. Several molecules are involved in regulation of ENaCs in bone formation, including nitride oxide synthases, voltage-sensitive calcium channels, and cyclooxygenase-2.
The pathway of ENaC involved in shear stress has an effect on stimulating osteoblasts even bone formation by estrogen interference.
综述上皮钠通道(ENaCs)诱导骨形成及调节机制的最新研究进展。
采用Medline、PubMed及中文文献索引检索2005年至2014年期间以英文或中文撰写的研究。关键词包括ENaC、骨、骨形成、骨坏死、雌激素和骨质疏松症。选取国内外近期文献中有关ENaC结构、ENaC在骨形成中作用机制的已发表文章的数据。
要求获取所有研究的摘要和全文。排除无法获取的研究以及未聚焦于关键词的研究。
ENaCs是由同源α、β和γ亚基组装而成的三聚体离子通道。ENaCs的晶体结构表明,ENaC具有位于三个亚基中心对称轴上的中央离子通道。ENaCs是蛋白酶敏感通道,其离子通道活性受蛋白水解反应调节。ENaCs的通道开放概率受蛋白酶、机械力和剪切应力调节。多种分子参与骨形成过程中ENaCs的调节,包括一氧化氮合酶、电压敏感性钙通道和环氧合酶-2。
ENaC参与剪切应力的途径通过雌激素干扰对成骨细胞甚至骨形成产生刺激作用。