Fibroblast growth factor 23 and the bone-vascular axis: lessons learned from animal studies

Am J Kidney Dis. 2012 Jan;59(1):135-44. doi: 10.1053/j.ajkd.2011.07.027. Epub 2011 Nov 8.


Calcification of arteries and cardiac valves is observed commonly in dialysis patients and represents a major determinant of the heightened cardiovascular risk observed during chronic kidney disease (CKD) progression. Recent advances from clinical and basic science studies suggest that vascular calcification should be considered a systemic disease in which pathologic processes occurring in the bone and kidney contribute to calcium deposition in the vasculature. Among the factors potentially involved in the vascular-bone axis dysregulation associated with CKD, there now is increasing interest in the role of the phosphaturic hormone fibroblast growth factor 23 (FGF-23). Increased FGF-23 plasma levels are observed with a decrease in kidney function and predict the risk of future cardiovascular mortality. However, clinical data are still unclear about whether a direct pathogenetic effect of FGF-23 on vascular/kidney/bone health exists. In the last few years, a series of basic science studies, performed using engineered mice, have contributed important pathophysiologic information about FGF-23 activities. This review summarizes findings from these studies and discusses the potential role of FGF-23 during the pathologic interplay between kidney, vessels, and bone in CKD.

Publication types

  • Case Reports
  • Review

MeSH terms

  • Animals
  • Blood Vessels / metabolism*
  • Bone and Bones / metabolism*
  • Chronic Disease
  • Fibroblast Growth Factors / physiology*
  • Humans
  • Kidney Diseases / complications*
  • Kidney Diseases / metabolism*
  • Male
  • Middle Aged
  • Vascular Calcification / etiology*


  • Fibroblast Growth Factors
  • fibroblast growth factor 23