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Biology of Fibroblast Growth Factor 23: From Physiology to Pathology

Marie Courbebaisse1,2, Beate Lanske1,3

  • 1Division of Bone and Mineral Research OMII, Harvard School of Dental Medicine, Boston, Massachusetts 02115.

Cold Spring Harbor Perspectives in Medicine
|August 6, 2017
PubMed

Insights

Fibroblast growth factor (FGF)23 regulates phosphate and vitamin D metabolism. High FGF23 levels, seen in kidney disease, can cause heart problems and increase mortality risk.

Area of Science:

  • Endocrinology
  • Nephrology
  • Cardiology

Background:

  • Fibroblast growth factor (FGF)23 is a hormone produced by bone cells.
  • FGF23 regulates phosphate and vitamin D metabolism by acting on the kidneys and parathyroid glands.
  • Its levels are often elevated in chronic kidney disease (CKD).

Purpose of the Study:

  • To review the physiology of FGF23.
  • To discuss the pathological consequences of abnormal FGF23 levels.
  • To highlight the association between high FGF23 and adverse health outcomes.

Main Methods:

  • Literature review of FGF23 physiology and pathology.
  • Analysis of FGF23's role in phosphate homeostasis.
  • Examination of FGF23's effects on renal and parathyroid function.

Main Results:

  • FGF23 inhibits renal phosphate reabsorption and calcitriol production.
  • It also suppresses parathyroid hormone (PTH) secretion.
  • Elevated FGF23 is linked to left ventricular hypertrophy (LVH) and increased mortality risk.

Conclusions:

  • FGF23 plays a critical role in mineral metabolism.
  • Dysregulation of FGF23 contributes to cardiovascular complications and mortality.
  • Understanding FGF23 is crucial for managing metabolic bone diseases and CKD complications.

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