Document details

Genetic disruption of NRF2 promotes the development of necroinflammation and liver fibrosis in a mouse model of HFE-hereditary hemochromatosis

Author(s): Duarte, T. ; Caldas, C. ; Santos, A. ; Silva-Gomes, S. ; Santos-Gonçalves, A. ; Martins, M. ; Porto, G. ; Lopes, J.

Date: 2017

Persistent ID: http://hdl.handle.net/10400.16/2180

Origin: Repositório Científico da Unidade Local de Saúde de Santo António (ULSSA)

Subject(s): Hepatocyte; Iron; Macrophage; Oxidative stress; Sideronecrosis


Description

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).

Document Type Journal article
Language English
Contributor(s) Repositório Científico da Unidade Local de Saúde de Santo António
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