Abstract
Purpose of reviewIron 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 findingsC-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.SummaryIn 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).
| Original language | English (US) |
|---|---|
| Pages (from-to) | 368-374 |
| Number of pages | 7 |
| Journal | Current opinion in nephrology and hypertension |
| Volume | 33 |
| Issue number | 4 |
| DOIs | |
| State | Published - Jul 1 2024 |
Funding
G.C. has nothing to disclose. V.D. received research funding from Akebia and from Vifor Pharma and consulting honoraria from Keryx Biopharmaceuticals, Vifor Pharma, Luitpold and Amgen outside of submitted work. This study was supported by grants from National Institute of Health to V.D. (R01DK102815, R01DK114158).
Keywords
- C-terminal fibroblast growth factor 23 peptides
- anemia of chronic kidney disease
- fibroblast growth factor 23
- hepcidin
- inflammation
- iron deficiency
ASJC Scopus subject areas
- Internal Medicine
- Nephrology