Elevated FGF23 Levels in Mice Lacking the Thiazide-Sensitive NaCl cotransporter (NCC)
Author:
Publisher
Springer Science and Business Media LLC
Subject
Multidisciplinary
Link
http://www.nature.com/articles/s41598-018-22041-1.pdf
Reference58 articles.
1. Hori, M., Shimizu, Y. & Fukumoto, S. Minireview: fibroblast growth factor 23 in phosphate homeostasis and bone metabolism. Endocrinology 152, 4–10 (2011).
2. Gattineni, J. et al. FGF23 decreases renal NaPi-2a and NaPi-2c expression and induces hypophosphatemia in vivo predominantly via FGF receptor 1. Am J Physiol Renal Physiol 297, F282–291 (2009).
3. Liu, S., Vierthaler, L., Tang, W., Zhou, J. & Quarles, L. D. FGFR3 and FGFR4 do not mediate renal effects of FGF23. J Am Soc Nephrol 19, 2342–2350 (2008).
4. Hu, M. C., Shiizaki, K., Kuro-o, M. & Moe, O. W. Fibroblast growth factor 23 and Klotho: physiology and pathophysiology of an endocrine network of mineral metabolism. Annu Rev Physiol 75, 503–533, https://doi.org/10.1146/annurev-physiol-030212-183727 (2013).
5. Andrukhova, O. et al. FGF23 acts directly on renal proximal tubules to induce phosphaturia through activation of the ERK1/2-SGK1 signaling pathway. Bone 51, 621–628, https://doi.org/10.1016/j.bone.2012.05.015 (2012).
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