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FGF23 signalling and physiology.

Bryan B Ho1, Clemens Bergwitz1

  • 1Department of Internal Medicine, Section Endocrinology, Yale University School of Medicine, New Haven, Connecticut, USA.

Journal of Molecular Endocrinology
|December 18, 2020
PubMed
Summary
This summary is machine-generated.

Fibroblast growth factor 23 (FGF23) regulates phosphate levels by inhibiting vitamin D synthesis and intestinal absorption. Its signaling pathways, both canonical and non-canonical, impact phosphate homeostasis and can lead to disorders.

Keywords:
CKDFGF receptorFGF23KLOTHOPTHerythropoetinhematopoesisironmineralisationphosphate homeostasisphosphate signalling

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Area of Science:

  • Endocrinology
  • Molecular Biology
  • Biochemistry

Background:

  • Fibroblast growth factor 23 (FGF23) is a key hormone regulating phosphate and vitamin D metabolism.
  • Its post-translational modifications, including phosphorylation and O-glycosylation, influence its secretion and biological activity.
  • FGF23 interacts with its receptor FGFR1c and co-receptor alpha-KLOTHO to mediate its effects.

Purpose of the Study:

  • To elucidate the intricate mechanisms of FGF23 synthesis, secretion, and signaling.
  • To understand the structural basis of FGF23-KLOTHO-FGFR1c complex formation.
  • To explore the physiological and pathophysiological consequences of FGF23 signaling.

Main Methods:

  • Analysis of FGF23 post-translational modifications (phosphorylation by FAM20C, O-glycosylation by GALNT3).
  • Investigation of FGF23 processing by proteases like FURIN and plasminogen activators.
  • Structural studies of FGF23 receptor-co-receptor interactions (KLOTHO-FGFR1c).
  • Examination of FGF23 signaling pathways (canonical: FRS2/RAS/RAF/MEK/ERK1/2; non-canonical: FGFR3/FGFR4/calcineurin/NFAT).

Main Results:

  • Post-translational modifications dictate FGF23 secretion as intact or fragmented forms, influencing biological activity.
  • The KLOTHO-FGFR1c complex forms a high-affinity binding site for FGF23.
  • Canonical FGF23 signaling reduces serum phosphate by inhibiting vitamin D synthesis and phosphate reabsorption.
  • Non-canonical signaling at high FGF23 levels is linked to cardiovascular complications.

Conclusions:

  • FGF23 processing and signaling pathways are critical for phosphate homeostasis.
  • Dysregulation of FGF23 signaling leads to hypophosphatemic or hyperphosphatemic disorders.
  • Aberrant FGF23 signaling, particularly non-canonical pathways, may contribute to cardiovascular disease in chronic kidney disease.