The parathyroid is a target organ for FGF23 in rats.

By I. Ben-Dov, Hillel Galitzer, Vardit Lavi-Moshayoff, R. Goetz, M. Kuro-o, M. Mohammadi, R. Sirkis, T. Naveh-Many, J. Silver. Journal of Clinical Investigation, 2007

977 citations recorded by the source corpus.

Subfields: Genetics, Molecular Biology, Nephrology

View Paper: https://www.semanticscholar.org/paper/a9f4d3f4f38866271b81499b814bb02d0bd30f6f

How researchers see this paper

The researchers whose trusted networks rank it highest, strongest advocate first. Every researcher gets a different order.

In Genetics

1. M. Mohammadi
2. N. Itoh
3. A. Beenken
4. D. Ornitz
5. M. Kuro-o

In Molecular Biology

1. M. Mohammadi
2. A. Beenken
3. N. Itoh
4. D. Ornitz
5. M. Kuro-o
6. Clemens Bergwitz
7. H. Jüppner
8. D. Mangelsdorf

In Nephrology

1. M. Mohammadi
2. A. Beenken

Citations in the corpus

• Fibroblast growth factors: from molecular evolution to roles in development, metabolism and disease. (2011, background): “organs including parathyroid gland and osteoblasts (73, 74).”
• Renal control of calcium, phosphate, and magnesium homeostasis. (2015, background): “Although FGF23 is known to suppress PTH in a nonuremic milieu, the parathyroid gland becomes resistant to FGF23 with progressive kidney disease, favoring PTH release and worsening of secondary hyperparathyroidism (59).”
• Research resource: Comprehensive expression atlas of the fibroblast growth factor system in adult mouse. (2010, background): “FGF23 acts on the parathyroid gland to suppress production and secretion of PTH (96).”
• The FGF family: biology, pathophysiology and therapy (2009, positive): “FGF23 also acts on the parathyroid gland to inhibit parathyroid hormone (PTH) secretio”
• Vitamin D and human health: lessons from vitamin D receptor null mice. (2008, background): “In addition, FGF23 suppresses the expression of PTH and 1 hydroxylase, thereby decreasing 1,25-(OH)2D levels (220, 221).”
• Regulation of Phosphate Homeostasis by PTH, Vitamin D, and FGF23 (2010, background): “FGF23 suppresses PTH mRNA synthesis and secretion in vitro and in vivo in an alpha klotho (KL)-dependent fashion (17).”
• Secondary hyperparathyroidism: pathogenesis, disease progression, and therapeutic options. (2011, background): “Investigation of the effect of FGF-23 on parathyroid function in normal and hyperplastic parathyroid glands showed that FGF-23 decreased PTH secretion (11) and cell proliferation and increased CaSR and VDR expression in normal glands (16).”