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).