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Iron metabolism genes shape the course of liver fibrosis in chronic hepatitis C: from disease progression to reversal after direct-acting antivirals treatment

datacite.subject.fosCiências Médicas
datacite.subject.sdg03:Saúde de Qualidade
dc.contributor.authorFerreira, Joana
dc.contributor.authorBicho, Manuel
dc.contributor.authorFaustino, Paula
dc.contributor.authorSerejo, Fátima
dc.date.accessioned2026-01-05T16:29:03Z
dc.date.available2026-01-05T16:29:03Z
dc.date.issued2025-09-26
dc.description.abstractChronic hepatitis C (CHC) is linked to iron overload, which significantly correlates with liver fibrosis. This study aimed to assess whether genetic polymorphisms related to iron metabolism are associated with fibrosis severity, predict improvement in fibrosis after HCV clearance with direct-acting antivirals (DAAs) and influence iron-related metabolic markers before treatment. A total of 329 CHC patients were included, 134 of whom received DAAs therapy. Liver fibrosis was assessed using transient elastography (FibroScan), and biochemical parameters were measured using standard methods. Eighteen genetic polymorphisms within five iron metabolism-related genes were analyzed using PCR-RFLP, endpoint genotyping, or next-generation sequencing (NGS). Before DAA treatment, patients with severe f ibrosis showed higher levels of serum iron (Fe), total iron-binding capacity (TIBC), and ferritin (Ft). SLC40A1 rs1439816_GG was associated with an increased risk of severe fibrosis. compared with GC or CC genotypes. SLC40A1 rs11568351_GC genotype was linked to a higher likelihood of remaining cirrhotic after HCV clearance. Elevated iron parameters were observed in carriers HFE C282Y_CY, TF IVS 11 G>A, and BMP2 570 A>T. Overall, polymorphisms in iron metabolism genes may influence both the severity of liver fibrosis prior to treatment, its regression after DAA therapy and the regulation of iron metabolism in CHC patients.eng
dc.description.sponsorshipThis research was funded by the Institute for Scientific Research Bento Rocha Cabral and Technology and Foundation for Science and Technology, PTDC/SAU-GMG/103307/2008; PhD scholarship PDE/BDE/114585/2016 and the APC was funded by the funds from the Foundation for Science and Technology to ISAMB (UID 04295—Instituto de Saúde Ambiental).
dc.identifier.citationViruses. 2025 Sep 26;17(10):1302. doi: 10.3390/v17101302
dc.identifier.doi10.3390/v17101302
dc.identifier.eissn1999-4915
dc.identifier.pmid41157574
dc.identifier.urihttp://hdl.handle.net/10400.18/10665
dc.language.isoeng
dc.peerreviewedyes
dc.publisherMDPI
dc.relationEnvironmental Health Institute
dc.relationPDE/BDE/114585/2016
dc.relationPTDC/SAU-GMG/103307/2008
dc.relation.hasversionhttps://www.mdpi.com/1999-4915/17/10/1302
dc.rights.urihttp://creativecommons.org/licenses/by/4.0/
dc.subjectChronic Hepatitis C
dc.subjectDirect-Acting Antivirals
dc.subjectFibrosis
dc.subjectGenetic Polymorphism
dc.subjectIron Metabolism
dc.subjectOxidative Stress
dc.subjectHepatite C
dc.subjectFibrose
dc.subjectMetabolismo do Ferro
dc.subjectHFE
dc.subjectPolimorfismos Genéticos
dc.subjectDoenças Genéticas
dc.titleIron metabolism genes shape the course of liver fibrosis in chronic hepatitis C: from disease progression to reversal after direct-acting antivirals treatmenteng
dc.typejournal article
dspace.entity.typePublication
oaire.awardTitleEnvironmental Health Institute
oaire.awardURIinfo:eu-repo/grantAgreement/FCT/6817 - DCRRNI ID/UID%2FDTP%2F04295%2F2013/PT
oaire.citation.issue10
oaire.citation.startPage1302
oaire.citation.titleViruses
oaire.citation.volume17
oaire.fundingStream6817 - DCRRNI ID
oaire.versionhttp://purl.org/coar/version/c_970fb48d4fbd8a85
project.funder.identifierhttp://doi.org/10.13039/501100001871
project.funder.nameFundação para a Ciência e a Tecnologia
relation.isProjectOfPublicationefdf215e-fa14-4759-a507-ae8a5946c71b
relation.isProjectOfPublication.latestForDiscoveryefdf215e-fa14-4759-a507-ae8a5946c71b

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