Is HMGB1 a New Indirect Marker for Revealing Fibrosis in Chronic Hepatitis and a New Therapeutic Target in Treatment?

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dc.authoridUyanik, Muhammet Hamidullah/0000-0002-0759-9832
dc.contributor.authorAlbayrak, Ayse
dc.contributor.authorUyanik, Muhammet H.
dc.contributor.authorCerrah, Serkan
dc.contributor.authorAltas, Sare
dc.contributor.authorDursun, Hakan
dc.contributor.authorDemir, Mehmet
dc.contributor.authorUslu, Hakan
dc.date.accessioned2024-09-18T21:05:08Z
dc.date.available2024-09-18T21:05:08Z
dc.date.issued2010
dc.departmentHatay Mustafa Kemal Üniversitesien_US
dc.description.abstractIn chronic hepatitis B virus (HBV) infection, inflammation-associated cytokines including proinflammatory cytokines are involved in the development and progression of liver fibrosis. The liver is a source of many cytokines that may influence liver function. High-mobility group box 1 (HMGB1) was identified as an inflammatory cytokine. HMGB1 is present in nuclei of all mammalian cells and is released both through active secretion from various cells and by passive release from necrotic cells. Here we explore the relationship between HMGB1 plasma levels and liver fibrosis. HMGB1 serum levels, HBV-DNA, and ALT values were significantly higher in patients with chronic HBV than in controls. In addition, HMGB1 serum levels were significantly higher in patients with low fibrosis (fibrosis score 1-2) compared to those with high fibrosis (fibrosis score 3-4). In the present study, we have shown that HMGB1 is a noninvasive, repeatable, and convenient marker for distinguishing advanced fibrosis from low fibrosis in chronic HBV patients. We believe that the inhibition of HMGB1 may reduce inflammation, apoptosis, and fibrosis, and may stop the progression of chronic liver disease. Furthermore, we are of the opinion that fibrotic progression in chronic liver patients may be prevented by the inhibition of HMGB1, and that this substance can be a new means of following chronic HBV treatment.en_US
dc.identifier.doi10.1089/vim.2010.0080
dc.identifier.endpage638en_US
dc.identifier.issn0882-8245
dc.identifier.issn1557-8976
dc.identifier.issue6en_US
dc.identifier.pmid21142449en_US
dc.identifier.scopus2-s2.0-78650081462en_US
dc.identifier.scopusqualityQ3en_US
dc.identifier.startpage633en_US
dc.identifier.urihttps://doi.org/10.1089/vim.2010.0080
dc.identifier.urihttps://hdl.handle.net/20.500.12483/13398
dc.identifier.volume23en_US
dc.identifier.wosWOS:000285093300011en_US
dc.identifier.wosqualityQ3en_US
dc.indekslendigikaynakWeb of Scienceen_US
dc.indekslendigikaynakScopusen_US
dc.indekslendigikaynakPubMeden_US
dc.language.isoenen_US
dc.publisherMary Ann Liebert, Incen_US
dc.relation.ispartofViral Immunologyen_US
dc.relation.publicationcategoryMakale - Uluslararası Hakemli Dergi - Kurum Öğretim Elemanıen_US
dc.rightsinfo:eu-repo/semantics/closedAccessen_US
dc.subjectMobility Group Box-1en_US
dc.subjectNeopterin Levelsen_US
dc.subjectLiver Ischemiaen_US
dc.subjectReleaseen_US
dc.subjectProteinen_US
dc.subjectInjuryen_US
dc.subjectAlphaen_US
dc.subjectDiseaseen_US
dc.subjectHmg-1en_US
dc.titleIs HMGB1 a New Indirect Marker for Revealing Fibrosis in Chronic Hepatitis and a New Therapeutic Target in Treatment?en_US
dc.typeArticleen_US

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