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dc.contributor.authorNascimento, José C.R.-
dc.contributor.authorMatos, Gabriella A.-
dc.contributor.authorPereira, Lianna C.-
dc.contributor.authorMourão, Anderson E.C.C.B.-
dc.contributor.authorSampaio, Aline M.-
dc.contributor.authorOriá, Reinaldo B.-
dc.contributor.authorToniuttoc, Pierluigi-
dc.identifier.citationNASCIMENTO, J. C. R. et al. Impact of apolipoprotein E genetic polymorphisms on liver disease: An essential review. Annals of Hepatology, v. 19, n. 1, p. 24-30, 2020. Disponível em: Acesso em: 20 abr. 2021.pt_BR
dc.description.abstractCirrhosis is an advanced stage of liver disease, compromising liver function with systemic health implications and poor quality of life. Hepatitis C virus (HCV) infection and alcoholic liver disease are the main causes of this pathology. However, since genetic factors may play a large role in the progression and severity of liver disease, and as apolipoprotein E (apoE) has been recognised to be mainly synthesised in the liver, apoE polymorphism studies are important to better understand the causal mechanisms in liver diseases. In this review, we summarise up-to-date studies addressing how apoE polymorphisms influence liver cirrhosis and liver transplantation outcomes and potential protective mechanisms. Although more clinical studies are needed to support these findings, the apoE 4 allele seems to be protective against the progression of liver cirrhosis in the majority of aetiologies and the postoperative serum apoE phenotype of the transplanted subject receptors was converted to that of the donor, indicating that >90% of apoE in plasma is synthesised in the hepatic system.pt_BR
dc.publisherAnnals of Hepatologypt_BR
dc.subjectApolipoproteínas Ept_BR
dc.subjectApolipoprotein Ept_BR
dc.subjectLiver cirrhosispt_BR
dc.subjectCirrose Hepáticapt_BR
dc.subjectLiver diseasespt_BR
dc.subjectLiver transplantationpt_BR
dc.subjectTransplante de Fígadopt_BR
dc.titleImpact of apolipoprotein E genetic polymorphisms on liver disease: an essential reviewpt_BR
dc.typeArtigo de Periódicopt_BR
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