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

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 ge...

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Detalhes bibliográficos
Autor principal: Duarte, T. (author)
Outros Autores: Caldas, C. (author), Santos, A. (author), Silva-Gomes, S. (author), Santos-Gonçalves, A. (author), Martins, M. (author), Porto, G. (author), Lopes, J. (author)
Formato: article
Idioma:eng
Publicado em: 2017
Assuntos:
Hepatocyte
Iron
Macrophage
Oxidative stress
Sideronecrosis
Texto completo:http://hdl.handle.net/10400.16/2180
País:Portugal
Oai:oai:repositorio.chporto.pt:10400.16/2180
Descrição
Resumo: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).

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