FGF23 at the crossroads of phosphate, iron economy and erythropoiesis.
Anemia, Iron-Deficiency
/ drug therapy
Bone and Bones
/ metabolism
Calcium
Erythropoiesis
/ genetics
Familial Hypophosphatemic Rickets
/ genetics
Ferric Compounds
/ adverse effects
Fibroblast Growth Factor-23
Fibroblast Growth Factors
/ genetics
Humans
Hypophosphatemia
/ chemically induced
Inflammation
/ genetics
Iron
/ metabolism
Maltose
/ adverse effects
Phosphates
/ metabolism
Protein Processing, Post-Translational
RNA, Messenger
/ metabolism
Renal Insufficiency, Chronic
/ genetics
Transcription, Genetic
Journal
Nature reviews. Nephrology
ISSN: 1759-507X
Titre abrégé: Nat Rev Nephrol
Pays: England
ID NLM: 101500081
Informations de publication
Date de publication:
01 2020
01 2020
Historique:
accepted:
24
07
2019
pubmed:
15
9
2019
medline:
17
4
2020
entrez:
15
9
2019
Statut:
ppublish
Résumé
Fibroblast growth factor 23 (FGF23) was initially characterized as an important regulator of phosphate and calcium homeostasis. New research advances demonstrate that FGF23 is also linked to iron economy, inflammation and erythropoiesis. These advances have been fuelled, in part, by the serendipitous development of two distinct FGF23 assays that can substitute for invasive bone biopsies to infer the activity of the three main steps of FGF23 regulation in bone: transcription, post-translational modification and peptide cleavage. This 'liquid bone biopsy for FGF23 dynamics' enables large-scale longitudinal studies of FGF23 regulation that would otherwise be impossible in humans. The balance between FGF23 production, post-translational modification and cleavage is maintained or perturbed in different hereditary monogenic conditions and in acquired conditions that mimic these genetic disorders, including iron deficiency, inflammation, treatment with ferric carboxymaltose and chronic kidney disease. Looking ahead, a deeper understanding of the relationships between FGF23 regulation, iron homeostasis and erythropoiesis can be leveraged to devise novel therapeutic targets for treatment of anaemia and states of FGF23 excess, including chronic kidney disease.
Identifiants
pubmed: 31519999
doi: 10.1038/s41581-019-0189-5
pii: 10.1038/s41581-019-0189-5
doi:
Substances chimiques
FGF23 protein, human
0
Ferric Compounds
0
Phosphates
0
RNA, Messenger
0
Fibroblast Growth Factors
62031-54-3
ferric carboxymaltose
6897GXD6OE
Maltose
69-79-4
Fibroblast Growth Factor-23
7Q7P4S7RRE
Iron
E1UOL152H7
Calcium
SY7Q814VUP
Types de publication
Journal Article
Review
Langues
eng
Sous-ensembles de citation
IM
Pagination
7-19Références
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