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Fibroblast growth factor (FGF) 23 regulates phosphate metabolism. High FGF23 levels, seen in kidney disease, can cause harm by affecting tissues lacking klotho, leading to pathologies.

Keywords:
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Area of Science:

  • Endocrinology
  • Molecular Biology
  • Pathology

Background:

  • Fibroblast growth factor (FGF) 23 is a key regulator of phosphate metabolism.
  • FGF23 typically signals through FGF receptors (FGFRs) with klotho as a co-receptor.
  • Klotho enhances FGF23 binding to FGFRs in target tissues like the kidney and parathyroid gland.

Purpose of the Study:

  • To describe FGF23 signaling and cellular events in tissues lacking klotho.
  • To discuss FGF23's potential role in widespread pathologic actions.
  • To explore the inhibitory effects of soluble klotho on FGF23-mediated signaling.

Main Methods:

  • Review of FGF23 signaling pathways.
  • Analysis of FGF23 effects in klotho-deficient contexts.
  • Discussion of clinical implications in chronic kidney disease.

Main Results:

  • FGF23 can signal independently of klotho at high concentrations.
  • Klotho-independent FGF23 signaling activates distinct downstream pathways.
  • This signaling is associated with pathologic cellular changes, including cardiac hypertrophy and inflammation.

Conclusions:

  • Elevated FGF23 in chronic kidney disease may drive pathologies by targeting klotho-lacking tissues.
  • FGF23 may act as a hormone with broad pathologic effects.
  • Soluble klotho might offer protective functions by inhibiting FGF23 signaling.