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Hfe actions in Kupffer cells are dispensable for hepatic and systemic iron metabolism.
Int. J. Mol. Sci. 24:10 (2023)
Mutations in the HFE/Hfe gene cause Hereditary Hemochromatosis (HH), a highly prevalent genetic disorder characterized by elevated iron deposition in multiple tissues. HFE acts in hepatocytes to control hepcidin expression, whereas HFE actions in myeloid cells are required for cell-autonomous and systemic iron regulation in aged mice. To address the role of HFE specifically in liver-resident macrophages, we generated mice with a selective Hfe deficiency in Kupffer cells (HfeClec4fCre). The analysis of the major iron parameters in this novel HfeClec4fCre mouse model led us to the conclusion that HFE actions in Kupffer cells are largely dispensable for cellular, hepatic and systemic iron homeostasis.
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Publication type
Article: Journal article
Document type
Scientific Article
Keywords
Hfe-hemochromatosis ; Kupffer Cells ; Hepcidin ; Iron ; Liver ; Macrophage; Gene; Mice
Language
english
Publication Year
2023
HGF-reported in Year
2023
ISSN (print) / ISBN
1661-6596
e-ISSN
1422-0067
Quellenangaben
Volume: 24,
Issue: 10
Article Number: 10
Publisher
MDPI
Publishing Place
Basel
Reviewing status
Peer reviewed
POF-Topic(s)
30203 - Molecular Targets and Therapies
Research field(s)
Enabling and Novel Technologies
PSP Element(s)
G-505200-003
Grants
Ulm University
DFG
DFG
WOS ID
000996779300001
Scopus ID
85160375386
PubMed ID
37240294
Erfassungsdatum
2023-10-06