Fatty Liver Disease 2004
DOI: 10.1002/9780470987438.ch10
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Cytokines and Inflammatory Recruitment in NASH: Experimental and Human Studies

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Cited by 3 publications
(6 citation statements)
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“…In conclusion, our study showed that the degree of liver fibrosis was significantly correlated with age, TNF-α and type IV collagen concentrations. The level of HA and type IV collagen could differentiate between mild fibrosis (stages 1-2) and advanced fibrosis (stages [3][4]. Further prospective studies with larger samples are needed.…”
Section: Resultsmentioning
confidence: 99%
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“…In conclusion, our study showed that the degree of liver fibrosis was significantly correlated with age, TNF-α and type IV collagen concentrations. The level of HA and type IV collagen could differentiate between mild fibrosis (stages 1-2) and advanced fibrosis (stages [3][4]. Further prospective studies with larger samples are needed.…”
Section: Resultsmentioning
confidence: 99%
“…Immunological mechanisms have an important role in the pathogenesis of NASH. Studies both in human and animal models have shown the role of pro‐inflammatory cytokines in causing hepatic injury 3 . The pathogenesis involved increased tumor necrosis factor‐α (TNF‐α) which was found in obese patients and contributed to the development of insulin resistance.…”
Section: Introductionmentioning
confidence: 99%
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“…Included in the spectrum of NAFLD are the relatively benign ‘simple steatosis’ and the more progressive ‘nonalcoholic steatohepatitis’ (NASH), the latter which may lead to cirrhosis in 15–25% of patients 3–6 . The pathogenesis of NASH is thought to be a multistep process in which steatosis (due to insulin resistance in most cases) is the initial step, and oxidative stress and cytokine mediated inflammation/apoptosis are important subsequent steps 7,8 . Among the various cytokines implicated in the pathogenesis of NASH, tumor necrosis factor alpha (TNFα) has received the greatest attention, and there is growing clinical evidence to support a pathophysiological role for this cytokine in NASH.…”
Section: Introductionmentioning
confidence: 99%
“…In contrast to genetically obese rodents, MCD rodents are neither leptin/leptin receptor deficient or obese, and they develop steatohepatitis rather than simple steatosis 30–32 . Leptin deficiency and obesity may influence the cytokine environment 7 and thus, potentially, hepatic sensitivity to LPS. It is therefore of interest to establish the effects of LPS in the MCD model of steatohepatitis in which leptin deficiency and obesity are absent.…”
Section: Introductionmentioning
confidence: 99%