Duarte, T.Caldas, C.Santos, A.Silva-Gomes, S.Santos-Gonçalves, A.Martins, M.Porto, G.Lopes, J.2017-09-042017-09-042017-04Redox Biol. 2017 Apr;11:157-1692213-2317http://hdl.handle.net/10400.16/2180In 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).engHepatocyteIronMacrophageOxidative stressSideronecrosisjournal article10.1016/j.redox.2016.11.013