PuSH - Publication Server of Helmholtz Zentrum München

Knoop, P.* ; Yilmaz, D.* ; Paganoni, R.* ; Steele-Perkins, P.* ; Gruber, A.* ; Akdogan, B. ; Zischka, H. ; Leopold, K.* ; Vujić Spasić, M.*

Hfe actions in Kupffer cells are dispensable for hepatic and systemic iron metabolism.

Int. J. Mol. Sci. 24:10 (2023)
DOI PMC
Creative Commons Lizenzvertrag
Open Access Gold as soon as Publ. Version/Full Text is submitted to ZB.
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.
Altmetric
Additional Metrics?
[➜Log in]
Edit extra informations Login
Publication type Article: Journal article
Document type Scientific Article
Corresponding Author
Keywords Hfe-hemochromatosis ; Kupffer Cells ; Hepcidin ; Iron ; Liver ; Macrophage; Gene; Mice
ISSN (print) / ISBN 1422-0067
e-ISSN 1661-6596
Journal International Journal of Molecular Sciences
Quellenangaben Volume: 24, Issue: 10 Pages: , Article Number: 10 Supplement: ,
Publisher MDPI
Publishing Place Basel
Non-patent literature Publications
Reviewing status Peer reviewed
Institute(s) Institute of Molecular Toxicology and Pharmacology (TOXI)
Grants Ulm University
DFG