Please use this identifier to cite or link to this item: http://hdl.handle.net/10400.16/2180
Title: Genetic disruption of NRF2 promotes the development of necroinflammation and liver fibrosis in a mouse model of HFE-hereditary hemochromatosis
Author: Duarte, T.
Caldas, C.
Santos, A.
Silva-Gomes, S.
Santos-Gonçalves, A.
Martins, M.
Porto, G.
Lopes, J.
Keywords: Hepatocyte
Iron
Macrophage
Oxidative stress
Sideronecrosis
Issue Date: Apr-2017
Publisher: Elsevier
Citation: Redox Biol. 2017 Apr;11:157-169
Abstract: In hereditary hemochromatosis, iron deposition in the liver parenchyma may lead to fibrosis, cirrhosis and hepatocellular carcinoma. Most cases are ascribed to a common mutation in the HFE gene, but the extent of clinical expression is greatly influenced by the combined action of yet unidentified genetic and/or environmental modifying factors. In mice, transcription factor NRF2 is a critical determinant of hepatocyte viability during exposure to acute dietary iron overload. We evaluated if the genetic disruption of Nrf2 would prompt the development of liver damage in Hfe(-/-) mice (an established model of human HFE-hemochromatosis).
Peer review: yes
URI: http://hdl.handle.net/10400.16/2180
DOI: 10.1016/j.redox.2016.11.013
ISSN: 2213-2317
Publisher Version: http://www.sciencedirect.com/science/article/pii/S2213231716302749?via%3Dihub
Appears in Collections:SHC - Artigos publicados em revistas indexadas na Medline

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