Iron Mining for Erythropoiesis.
erythroferrone
erythropoiesis
hepcidin
hypoxia
iron metabolism
Journal
International journal of molecular sciences
ISSN: 1422-0067
Titre abrégé: Int J Mol Sci
Pays: Switzerland
ID NLM: 101092791
Informations de publication
Date de publication:
10 May 2022
10 May 2022
Historique:
received:
15
04
2022
revised:
05
05
2022
accepted:
09
05
2022
entrez:
28
5
2022
pubmed:
29
5
2022
medline:
1
6
2022
Statut:
epublish
Résumé
Iron is necessary for essential processes in every cell of the body, but the erythropoietic compartment is a privileged iron consumer. In fact, as a necessary component of hemoglobin and myoglobin, iron assures oxygen distribution; therefore, a considerable amount of iron is required daily for hemoglobin synthesis and erythroid cell proliferation. Therefore, a tight link exists between iron metabolism and erythropoiesis. The liver-derived hormone hepcidin, which controls iron homeostasis via its interaction with the iron exporter ferroportin, coordinates erythropoietic activity and iron homeostasis. When erythropoiesis is enhanced, iron availability to the erythron is mainly ensured by inhibiting hepcidin expression, thereby increasing ferroportin-mediated iron export from both duodenal absorptive cells and reticuloendothelial cells that process old and/or damaged red blood cells. Erythroferrone, a factor produced and secreted by erythroid precursors in response to erythropoietin, has been identified and characterized as a suppressor of hepcidin synthesis to allow iron mobilization and facilitate erythropoiesis.
Identifiants
pubmed: 35628152
pii: ijms23105341
doi: 10.3390/ijms23105341
pmc: PMC9140467
pii:
doi:
Substances chimiques
Hemoglobins
0
Hepcidins
0
Iron
E1UOL152H7
Types de publication
Journal Article
Review
Langues
eng
Sous-ensembles de citation
IM
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