Fibroblast growth factor 23 is pumping iron: C-terminal-fibroblast growth factor 23 cleaved peptide and its function in iron metabolism.
Curr Opin Nephrol Hypertens
; 33(4): 368-374, 2024 07 01.
Article
em En
| MEDLINE
| ID: mdl-38661434
ABSTRACT
PURPOSE OF REVIEW Iron deficiency regulates the production of the bone-derived phosphaturic hormone fibroblast growth factor 23 (FGF23) but also its cleavage, to generate both intact (iFGF23) and C-terminal (Cter)-FGF23 peptides. Novel studies demonstrate that independently of the phosphaturic effects of iFGF23, Cter-FGF23 peptides play an important role in the regulation of systemic iron homeostasis. This review describes the complex interplay between iron metabolism and FGF23 biology. RECENT FINDINGS:
C-terminal (Cter) FGF23 peptides antagonize inflammation-induced hypoferremia to maintain a pool of bioavailable iron in the circulation. A key mechanism proposed is the down-regulation of the iron-regulating hormone hepcidin by Cter-FGF23.SUMMARY:
In this manuscript, we discuss how FGF23 is produced and cleaved in response to iron deficiency, and the principal functions of cleaved C-terminal FGF23 peptides. We also review possible implications anemia of chronic kidney disease (CKD).
Texto completo:
1
Base de dados:
MEDLINE
Assunto principal:
Fatores de Crescimento de Fibroblastos
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Hepcidinas
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Fator de Crescimento de Fibroblastos 23
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Ferro
Idioma:
En
Ano de publicação:
2024
Tipo de documento:
Article