Understanding the contribution of iron overload in non-alcoholic fatty liver disease: identification of cellular players and potential molecular therapeutic targets

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

Publication . Duarte, T.; Caldas, C.; Santos, A.; Silva-Gomes, S.; Santos-Gonçalves, A.; Martins, M.; Porto, G.; Lopes, J.

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).

2017-04Artigo científico

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Entidade financiadora

Fundação para a Ciência e a Tecnologia

Programa de financiamento

5876-PPCDTI

Número da atribuição

PTDC/BIM-MET/0739/2012