Non-renal-Related Mechanisms of FGF23 Pathophysiology
Author:
Publisher
Springer Science and Business Media LLC
Subject
Endocrinology, Diabetes and Metabolism
Link
http://link.springer.com/article/10.1007/s11914-018-0492-2/fulltext.html
Reference65 articles.
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2. Gattineni J, Bates C, Twombley K, Dwarakanath V, Robinson ML, Goetz R, et al. FGF23 decreases renal NaPi-2a and NaPi-2c expression and induces hypophosphatemia in vivo predominantly via FGF receptor 1. Am J Physiol Ren Physiol. 2009;297(2):F282–91. https://doi.org/10.1152/ajprenal.90742.2008 .
3. Bai XY, Miao D, Goltzman D, Karaplis AC. The autosomal dominant hypophosphatemic rickets R176Q mutation in fibroblast growth factor 23 resists proteolytic cleavage and enhances in vivo biological potency. J Biol Chem. 2003;278(11):9843–9. https://doi.org/10.1074/jbc.M210490200 .
4. Shimada T, Hasegawa H, Yamazaki Y, Muto T, Hino R, Takeuchi Y, et al. FGF-23 is a potent regulator of vitamin D metabolism and phosphate homeostasis. J Bone Miner Res. 2004;19(3):429–35. https://doi.org/10.1359/jbmr.0301264 .
5. Christakos S, Dhawan P, Verstuyf A, Verlinden L, Carmeliet G. Vitamin D: Metabolism, molecular mechanism of action, and pleiotropic effects. Physiol Rev. 2016;96(1):365–408. https://doi.org/10.1152/physrev.00014.2015 .
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