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From fatty liver to fibrosis: A tale of -second hit-

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dc.contributor.authorBasaranoglu, METİN
dc.contributor.authorBasaranoglu, GÖKÇEN
dc.contributor.authorSenturk, HAKAN
dc.contributor.institutionauthorBAŞARANOĞLU, METİN
dc.contributor.institutionauthorBAŞARANOĞLU, GÖKÇEN
dc.contributor.institutionauthorŞENTÜRK, HAKAN
dc.date.accessioned2019-10-05T12:45:08Z
dc.date.available2019-10-05T12:45:08Z
dc.date.issued2013-02-28
dc.description.abstractAlthough much is known about how fat accumulates in the liver, much remains unknown about how this causes sustained hepatocellular injury. The consequences of injury are recognized as nonalcoholic steatohepatitis (NASH) and progressive fibrosis. The accumulation of fat within the hepatocytes sensitizes the liver to injury from a variety of causes and the regenerative capacity of a fatty liver is impaired. An additional stressor is sometimes referred to as a “second hit” in a paradigm that identifies the accumulation of fat as the “first hit”. Possible candidates for the second hit include increased oxidative stress, lipid peroxidation and release of toxic products such as malondialdehyde and 4-hydroxynonenal, decreased antioxidants, adipocytokines, transforming growth factor (TGF)-β, Fas ligand, mitochondrial dysfunction, fatty acid oxidation by CYPs (CYP 2E1, 4A10 and 4A14), and peroxisomes, excess iron, small intestinal bacterial overgrowth, and the generation of gut-derived toxins such as lipopolysaccharide and ethanol. Oxidative stress is one of the most popular proposed mechanisms of hepatocellular injury. Previous studies have specifically observed increased plasma and tissue levels of oxidative stress markers and lipid peroxidation products, with reduced hepatic and plasma levels of antioxidants. There is also some indirect evidence of the benefit of antioxidants such as vitamin E, S-adenosylmethionine, betaine, phlebotomy to remove iron, and N-acetylcysteine in NASH. However, a causal relationship or a pathogenic link between NASH and oxidative stress has not been established so far. A number of sources of increased reactive oxygen species production have been established in NASH that include proinflammatory cytokines such as tumor necrosis factor (TNF)-α, iron overload, overburdened and dysfunctional mitochondria, CYPs, and peroxisomes. Briefly, the pathogenesis of NASH is multifactorial and excess intracellular fatty acids, oxidant stress, ATP depletion, and mitochondrial dysfunction are important causes of hepatocellular injury in the steatotic liver.en
dc.identifier10.1111/and.12071
dc.identifier.citationBasaranoglu M., Basaranoglu G., Senturk H., -From fatty liver to fibrosis: A tale of -second hit-, WORLD JOURNAL OF GASTROENTEROLOGY, cilt.19, ss.1158-1165, 2013
dc.identifier.doi10.3748/wjg.v19.i8.1158
dc.identifier.pubmed23483818
dc.identifier.scopus84874620716
dc.identifier.trdizintrdizin
dc.identifier.urihttps://hdl.handle.net/20.500.12645/482
dc.identifier.urihttps://www.ncbi.nlm.nih.gov/pmc/articles/PMC3587471/
dc.identifier.wosWOS:000315521700002
dc.language.isoen
dc.rightsinfo:eu-repo/semantics/openAccessen
dc.subjectFatty liver
dc.subjectOxidative stress
dc.subjectFibrosis
dc.subjectNonalcoholic fatty liver diseases
dc.subjectNonalcoholic steatohepatitis
dc.titleFrom fatty liver to fibrosis: A tale of -second hit-
dc.typeArticle
dspace.entity.typePublication
local.article.journalnameANDROLOGIA
local.avesis.id08e91ff4-07dc-41c9-ae4b-cc5fa577e6a0
local.avesis.response352
local.org.facultyTıp Fakültesi
local.publication.isinternational1
relation.isAuthorOfPublication8a7b20a3-6e3e-4a44-acbf-16854071f233
relation.isAuthorOfPublicationb508b903-f47b-4fb9-b3cb-7765e85e885a
relation.isAuthorOfPublication278fcf63-3b92-4368-bff6-f140ebd9aeb3
relation.isAuthorOfPublication.latestForDiscovery278fcf63-3b92-4368-bff6-f140ebd9aeb3
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