Gene expression of tumor necrosis factor α and TNF‐receptors, p55 and p75, in nonalcoholic steatohepatitis patients
By J. Crespo, A. Cayón, P. Fernández-Gil, M. Hernández‐Guerra, M. Mayorga, A. Domínguez‐Díez, José Carlos Fernández-Escalante, F. Pons‐Romero. 2001
660 citations recorded by the source corpus.
Subfields: Animal Science and Zoology, Epidemiology, Surgery
View Paper: https://www.semanticscholar.org/paper/70a7127c653f02996bcc96755d88740e80782c3f
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In Epidemiology
- Eran Elinav
- Gerald I. Shulman
- Ali Canbay
- M. Trauner
- Rebekka A. Hannivoort
- G. Gerken
- L. Bechmann
- P. Newsome
In Surgery
Citations in the corpus
- Pathogenesis of non-alcoholic fatty liver disease (2009, background): “Both serum and hepatic levels of TNF-a are elevated in patients with NASH,(43,44) and levels correlate with histological severity.(45) In addition to its proinflammatory effects, TNF-a promotes IR.”
- The interaction of hepatic lipid and glucose metabolism in liver diseases. (2012, background): “FAs induce the production of TNFa, and hepatic TNF receptor expression correlates with the disease severity in NAFLD [101].”
- Mouse models in non‐alcoholic fatty liver disease and steatohepatitis research (2006, background): “Studies also demonstrate greater expression of TNFa and TNFa type 1 receptor in patients with steatohepatitis than those with steatosis alone (Crespo et al. 2001; Kugelmas et al. 2003).”
- The multiple-hit pathogenesis of non-alcoholic fatty liver disease (NAFLD). (2016, neutral): “of liver damage [57].”
- Systemic inflammation in nonalcoholic fatty liver disease is characterized by elevated levels of CCL2. (2006, background): “Thus, while several studies have explored the role of TNF-a in these disorders [7,10,11], much less focus has been directed against the possible involvement of other inflammatory mediators.”
- Inflammasome-mediated dysbiosis regulates progression of NAFLD and obesity (2012, background): “Pro-inflammatory cytokines, and in particular TNF-a, a downstream cytokine of TLR signalling, are known to contribute to progression of hepatic steatosis to steatohepatitis and eventually hepatic fibrosis in a number of animal models and in human patient”