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Fibroblast growth factor 23 acts on the parathyroid to decrease parathyroid hormone secretion.

Hillel Galitzer¹, Iddo Ben-Dov, Vardit Lavi-Moshayoff

¹Minerva Center for Calcium and Bone Metabolism, Nephrology Services, Hadassah Hebrew University Medical Center, Jerusalem, Israel.

Current Opinion in Nephrology and Hypertension

|July 29, 2008

Summary

This summary is machine-generated.

Fibroblast growth factor 23 (FGF23) regulates phosphate and vitamin D. FGF23 acts on the parathyroid gland to decrease parathyroid hormone, impacting calcium and phosphate balance.

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Area of Science:

Endocrinology
Mineral Metabolism
Bone Biology

Background:

Fibroblast growth factor 23 (FGF23) is a key hormone regulating phosphate homeostasis.
FGF23 plays a crucial role in the bone-kidney axis, influencing bone mineralization and phosphate reabsorption.
Recent findings indicate the presence of FGF23 receptors in the parathyroid gland.

Purpose of the Study:

To elucidate the action of fibroblast growth factor 23 (FGF23) on the parathyroid gland.
To describe the FGF23-mediated regulation of parathyroid hormone (PTH).

Main Methods:

Review of existing literature on FGF23 signaling and parathyroid function.
Analysis of in vivo and in vitro studies investigating FGF23 effects on parathyroid hormone mRNA and secretion.

Main Results:

Fibroblast growth factor 23 (FGF23) inhibits renal phosphate reabsorption and calcitriol production.
FGF23 binds to the Klotho-FGFR1c complex in target tissues, including the parathyroid.
FGF23 activation of the MAPK pathway in the parathyroid leads to decreased PTH gene expression and secretion.

Conclusions:

Fibroblast growth factor 23 (FGF23) acts on the parathyroid gland via the Klotho-FGFR1c receptor, reducing PTH levels.
This FGF23-mediated reduction in PTH contributes to regulating phosphate, calcium, and calcitriol homeostasis.
A complex hormonal network involving FGF23, PTH, and calcitriol balances mineral and bone metabolism.