Linking nonalcoholic fatty liver disease to hepatocellular carcinoma: from bedside to bench and back

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dc.contributor.authorYilmaz, Yusuf
dc.contributor.authorColak, Yasar
dc.contributor.authorKurt, Ramazan
dc.contributor.authorSenates, Ebubekir
dc.contributor.authorEren, Fatih
dc.date.accessioned2024-04-24T17:14:34Z
dc.date.available2024-04-24T17:14:34Z
dc.date.issued2013
dc.departmentDicle Üniversitesien_US
dc.description.abstractAims and background. Nonalcoholic fatty liver disease (NAFLD) and hepatocellular carcinoma (HCC) are two major causes of liver disease worldwide. Epidemiological and clinical data have clearly demonstrated that NAFLD and its associated metabolic abnormalities are a risk factor for HCC. Traditionally, the mechanisms whereby NAFLD acts as a risk for HCC are believed to include replicative senescence of steatotic hepatocytes and compensatory hyperplasia of progenitor cells as a reaction to chronic hepatic injury. Recent years have witnessed significant advances in our understanding of the mechanisms underlying the link between NAFLD and HCC. Methods. In the present review, we provide an update on the pathophysiological pathways linking NAFLD and its associated metabolic derangements to malignant hepatic transformation, with a special focus on insulin resistance, adipokines, inflammation, and angiogenesis. We will also discuss the potential therapeutic implications that such molecular links carry. Results. Although treating NAFLD could reduce the risk of malignant hepatic transformation, no long-term studies focusing on this issue have been conducted thus far. Insulin resistance, inflammation as well as derangements in adipokines and angiogenic factors associated with NAFLD are closely intertwined with the risk of developing HCC. Conclusions. Traditional therapeutic approaches in NAFLD including metformin and statins may theoretically reduce the risk of HCC by acting on common pathophysiological pathways shared by NAFLD and HCC.en_US
dc.identifier.doi10.1177/030089161309900102
dc.identifier.endpage16en_US
dc.identifier.issn0300-8916
dc.identifier.issn2038-2529
dc.identifier.issue1en_US
dc.identifier.pmid23548993
dc.identifier.scopus2-s2.0-84878161368
dc.identifier.scopusqualityQ3
dc.identifier.startpage10en_US
dc.identifier.urihttps://doi.org/10.1177/030089161309900102
dc.identifier.urihttps://hdl.handle.net/11468/18068
dc.identifier.volume99en_US
dc.identifier.wosWOS:000322747800002
dc.identifier.wosqualityN/A
dc.indekslendigikaynakWeb of Science
dc.indekslendigikaynakScopus
dc.indekslendigikaynakPubMed
dc.language.isoenen_US
dc.publisherSage Publications Ltden_US
dc.relation.ispartofTumori Journal
dc.relation.publicationcategoryMakale - Uluslararası Hakemli Dergi - Kurum Öğretim Elemanıen_US
dc.rightsinfo:eu-repo/semantics/closedAccessen_US
dc.subjectNonalcoholic Fatty Liver Diseaseen_US
dc.subjectHepatocellular Carcinomaen_US
dc.subjectInsulin Resistanceen_US
dc.subjectAdipokinesen_US
dc.titleLinking nonalcoholic fatty liver disease to hepatocellular carcinoma: from bedside to bench and backen_US
dc.titleLinking nonalcoholic fatty liver disease to hepatocellular carcinoma: from bedside to bench and back
dc.typeReview Articleen_US

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