Estrogens and bone disease in chronic kidney disease: role of FGF23

Curr Opin Nephrol Hypertens. 2010 Jul;19(4):354-8. doi: 10.1097/MNH.0b013e328338f508.

Abstract

Purpose of review: To describe the direct and indirect effects of estrogen on bone with special emphasis on the analysis of the recent findings related to the putative role of FGF23 in the estrogen-dependent parathyroid hormone (PTH) suppression.

Recent findings: Estrogens act directly on bone cells, downregulating osteoclast precursors and differentiation, increasing osteoclast apoptosis and stimulating osteoblast proliferation and differentiation. However, estrogens can also act indirectly on bone, modulating the calcium-phosphorus-vitamin D-PTH axis. It has been recently demonstrated that estrogens suppress PTH synthesis and secretion in a dose-dependent manner and reduce serum calcitriol and phosphorus levels by an indirect mechanism. In-vivo and in-vitro experiments demonstrated that FGF23 positively correlated, also in a dose-dependent manner, with the dose of estrogens and with the observed changes in calcitriol and phosphorus.

Summary: These new findings support the importance of the indirect effects of estrogens on bone, suggesting a role for FGF23 in the regulation of PTH by estrogens.

Publication types

  • Research Support, Non-U.S. Gov't
  • Review

MeSH terms

  • Animals
  • Bone Diseases / etiology
  • Bone Diseases / metabolism*
  • Bone and Bones / drug effects
  • Bone and Bones / metabolism
  • Estrogens / metabolism*
  • Estrogens / pharmacology
  • Estrogens / physiology
  • Fibroblast Growth Factors / metabolism*
  • Humans
  • Kidney Failure, Chronic / complications
  • Kidney Failure, Chronic / metabolism*
  • Parathyroid Hormone / physiology
  • Signal Transduction
  • Vitamin D / physiology

Substances

  • Estrogens
  • Parathyroid Hormone
  • Vitamin D
  • Fibroblast Growth Factors
  • fibroblast growth factor 23