2012
DOI: 10.3389/fphys.2012.00248
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Liver Fibrogenesis in Non-Alcoholic Steatohepatitis

Abstract: Non-alcoholic fatty liver disease (NAFLD) is emerging as one of the most common chronic liver diseases in developed western countries. Non-alcoholic steatohepatitis (NASH) is the most severe form of NAFLD, and can progress to more severe forms of liver disease, including fibrosis, cirrhosis, and even hepatocellular carcinoma. The activation of hepatic stellate cells plays a critical role in NASH-related fibrogenesis. Multiple factors, such as insulin resistance, oxidative stress, pro-inflammatory cytokines and… Show more

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Cited by 32 publications
(29 citation statements)
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“…31 The relationship of adipokines with NAFLD has been extensively investigated in several previous studies, 32,33 but the published reports have yielded conflicting results regarding the role of adipokines in the pathogenesis of NAFLD. 34,35 In the present study, we found a significant association of IL-6 with lobular inflammation and fibrosis in NAFLD. So, our results are in line with current scientific knowledge regarding this issue.…”
Section: Ercin Et Almentioning
confidence: 74%
“…31 The relationship of adipokines with NAFLD has been extensively investigated in several previous studies, 32,33 but the published reports have yielded conflicting results regarding the role of adipokines in the pathogenesis of NAFLD. 34,35 In the present study, we found a significant association of IL-6 with lobular inflammation and fibrosis in NAFLD. So, our results are in line with current scientific knowledge regarding this issue.…”
Section: Ercin Et Almentioning
confidence: 74%
“…In one model, Otsuka Long-Evans Tokishima Fatty (OLETF) rats were fed with a methionine-and choline-deficient (MCD) diet [56,94]. In this model a diet mixed with silymarin 0.5 % w/w (approx.…”
Section: Animal Modelsmentioning
confidence: 99%
“…IL-6 activates signal transducer and activator of transcription 3, which induces cell proliferation and antiapoptotic mechanisms. TNF-α activates pro-oncogenic pathways, including c-Jun N-terminal kinase, nuclear factor kappa-light-chain-enhancer of activated B cells, mammalian target of rapamycin, and the extracellular signal-regulated kinases 2932. interestingly, several studies indicated that both dietary and genetic obesity could promote liver inflammation and tumorigenesis by enhancing IL-6 and TNF-α expression 3336…”
Section: Introductionmentioning
confidence: 99%