颠覆肾性骨营养不良的定论：FGF23 对成骨细胞 β-连环蛋白通路的直接作用。
Turning over renal osteodystrophy dogma: direct actions of FGF23 on osteoblast β-catenin pathway.
机构信息
PreciThera, Montreal, Quebec, Canada.
Medicine Master Degree Program, Universidade Nove de Julho, Universidade Nove de Julho, São Paulo, Brazil; Nephrology Division, Universidade de São Paulo, São Paulo, Brazil.
出版信息
Kidney Int. 2016 Jul;90(1):17-20. doi: 10.1016/j.kint.2016.03.028.
Although recognized as a major complication of chronic kidney disease (CKD), the pathophysiology of the CKD-related mineral and bone disorder (CKD-MBD) is not completely understood. Recently, the inhibition of Wnt/β-catenin pathway in osteocytes by sclerostin has been shown to play a role in CKD-MBD. The study by Carrilo-Lopez et al. confirms this inhibition in an experimental model of CKD. Moreover, they describe direct actions of FGF23-Klotho on osteoblasts, increasing the expression of DKK1, another Wnt/β-catenin pathway inhibitor.
虽然被认为是慢性肾脏病（CKD）的主要并发症，但 CKD 相关的矿物质和骨代谢紊乱（CKD-MBD）的病理生理学尚未完全阐明。最近，骨细胞中硬骨素对 Wnt/β-catenin 通路的抑制作用被证明在 CKD-MBD 中起作用。Carrilo-Lopez 等人的研究在 CKD 的实验模型中证实了这种抑制作用。此外，他们描述了 FGF23-Klotho 对成骨细胞的直接作用，增加了另一种 Wnt/β-catenin 通路抑制剂 DKK1 的表达。
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