Fibroblast growth factor 23 and the bone-vascular axis: lessons learned from animal studies.
Am J Kidney Dis
; 59(1): 135-44, 2012 Jan.
Article
en En
| MEDLINE
| ID: mdl-22070851
ABSTRACT
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.
Texto completo:
1
Bases de datos:
MEDLINE
Asunto principal:
Vasos Sanguíneos
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Huesos
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Calcificación Vascular
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Factores de Crecimiento de Fibroblastos
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Enfermedades Renales
Tipo de estudio:
Prognostic_studies
Límite:
Animals
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Humans
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Male
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Middle aged
Idioma:
En
Revista:
Am J Kidney Dis
Año:
2012
Tipo del documento:
Article
País de afiliación:
Italia