Effects of klotho deletion from bone during chronic kidney disease.
Effects of klotho deletion from bone during chronic kidney disease.
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DOI：
10.1016/j.bone.2017.02.006
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发表时间：
2017-07
期刊：
影响因子：
4.1
通讯作者：
Lanske B
中科院分区：
文献类型：
--
作者：
Kaludjerovic J;Komaba H;Lanske B
Klotho是一种I型跨膜蛋白，作为FGF23的允许共受体，有助于维持适当的矿物质代谢。在Klotho或Fgf23基因中携带功能丧失突变的小鼠会产生许多相似的表型，包括骨质疏松症。基于这些观察结果，假设Klotho和Fgf23缺失小鼠的骨表型可能通过共同的信号传导途径介导。抗体特异性的最新改进表明，产生FGF 23的成骨细胞和骨细胞也表达少量的膜Klotho。但是，Klotho在骨骼中的作用在很大程度上仍然不清楚。在这篇综述中，我们总结了文献，并表明Klotho在骨中具有FGF23依赖性和独立性作用。
Klotho is a type I transmembrane protein that acts as a permissive co-receptor for FGF23 and helps to maintain proper mineral metabolism. Mice carrying a loss-of-function mutation in either the Klotho or Fgf23 gene develop many similar phenotypes including osteoporosis. Based on these observations it was hypothesized that the bone phenotypes in Klotho- and Fgf23-null mice may be mediated through a common signaling pathway. Recent improvements in antibody specificity have shown that osteoblasts and osteocytes, which produce FGF23, also express low amount of membrane Klotho. But, the role of Klotho in bone is still largely unclear. In this review we summarize the literature and show that Klotho has an FGF23 dependent and independent effect in bone.