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Hepatitis C Virus: An Overview of Its Chronic Impact on Liver Function, Metabolic Dysregulation, Inflammatory–Oxidative Pathogenesis and Epigenetic Memory

datacite.subject.fosCiências Médicas
datacite.subject.sdg03:Saúde de Qualidade
dc.contributor.authorFerreira, Joana
dc.contributor.authorCaldeira, João
dc.contributor.authorBicho, Manuel
dc.contributor.authorFaustino, Paula
dc.contributor.authorSerejo, Fátima
dc.date.accessioned2026-09-30T15:17:24Z
dc.date.available2026-09-30T15:17:24Z
dc.date.issued2026-04-16
dc.descriptionThis article belongs to the Special Issue Advancements in Inflammatory and Oxidative Disease Research.
dc.description.abstractHepatitis C virus (HCV) infection is a global health concern, chronically affecting over 71 million people. It primarily targets the liver but also causes systemic complications through inflammation, oxidative stress, and metabolic dysregulation. HCV is a highly variable RNA virus with six major genotypes that are mainly transmitted via blood. Often asymptomatic, the infection progresses silently to chronic hepatitis C (CHC), which can lead to fibrosis, cirrhosis, and hepatocellular carcinoma (HCC). Direct-acting antivirals (DAAs) have revolutionized treatment, achieving cure rates above 95%, improving liver function, reversing fibrosis, and normalizing metabolism. HCV disrupts iron metabolism by suppressing hepcidin, causing iron overload and oxidative stress. It also alters lipid metabolism, inducing steatosis, and affects glucose metabolism, contributing to insulin resistance and type 2 diabetes. DAAs improve these metabolic outcomes. HCV promotes oxidative stress via viral proteins, damaging liver cells and DNA and triggering inflammation and fibrogenesis. Even post-cure, oxidative stress and iron overload may continue to drive disease progression. Genetic and epigenetic factors influence fibrosis progression and HCC risk. Despite a sustained virologic response (SVR), patients with advanced liver damage remain at risk for HCC and metabolic diseases, highlighting the need for continued monitoring and personalized post-treatment care.eng
dc.description.sponsorshipThis research was funded by the Institute for Scientific Research Bento Rocha Cabral and Technology and the 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/04295/2025, UID/PRR/04295/2025, and UID/PRR2/04295/2025).
dc.identifier.citationInt J Mol Sci. 2026 Apr 16;27(8):3559. doi: 10.3390/ijms27083559
dc.identifier.doi10.3390/ijms27083559
dc.identifier.eissn1422-0067
dc.identifier.issn1661-6596
dc.identifier.pmid42074199
dc.identifier.urihttp://hdl.handle.net/10400.18/11358
dc.language.isoeng
dc.peerreviewedyes
dc.publisherMDPI
dc.relationPTDC/SAU-GMG/103307/2008
dc.relationPDE/BDE/114585/2016
dc.relationUID/04295/2025
dc.relationUID/PRR/04295/2025
dc.relationUID/PRR2/04295/2025
dc.relation.hasversionhttps://www.mdpi.com/1422-0067/27/8/3559
dc.rights.urihttp://creativecommons.org/licenses/by/4.0/
dc.subjectChronic Hepatitis C
dc.subjectInflammatory–Oxidative Pathogenesis
dc.subjectLiver Damage
dc.subjectMetabolic Dysregulation
dc.subjectHepatite C Crónica
dc.subjectDoenças Genéticas
dc.subjectMetabolismo do Ferro
dc.titleHepatitis C Virus: An Overview of Its Chronic Impact on Liver Function, Metabolic Dysregulation, Inflammatory–Oxidative Pathogenesis and Epigenetic Memoryeng
dc.typejournal article
dspace.entity.typePublication
oaire.citation.issue8
oaire.citation.startPage3559
oaire.citation.titleInternational Journal of Molecular Sciences
oaire.citation.volume27
oaire.versionhttp://purl.org/coar/version/c_970fb48d4fbd8a85

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