Cytokines in alcoholic and nonalcoholic steatohepatitis.

By Herbert Tilg, A. Diehl. New England Journal of Medicine, 2000

978 citations recorded by the source corpus.

Subfields: Epidemiology, Genetics, Hepatology

View Paper: https://www.semanticscholar.org/paper/0ab50a8733cd3421744e5705e9c83feaba9df76b

How researchers see this paper

The researchers whose trusted networks rank it highest, strongest advocate first. Every researcher gets a different order.

In Epidemiology

1. G. Targher
2. Herbert Tilg
3. Q. Anstee
4. L. Adams
5. Robert D. Goldin
6. Z. Younossi
7. Christopher D. Byrne

In Genetics

1. Q. Anstee
2. Herbert Tilg

In Hepatology

1. Herbert Tilg
2. Q. Anstee
3. Robert D. Goldin
4. G. Targher

Citations in the corpus

• The changing faces of glutathione, a cellular protagonist. (2003, background): “Unfortunately, there is no approved therapy for ASH/NASH, which reflects our incomplete understanding of the underlying mechanisms (Tilg and Diehl, 2000; Angulo and Lindor, 2002; Brunt, 2004).”
• Acute-on-chronic liver failure: consensus recommendations of the Asian Pacific Association for the study of the liver (APASL) (2009, background): “Proinflammatory cytokines are believed to mediate hepatic inflammation, apoptosis, and necrosis of liver cells; cholestasis; and fibrosis [32, 45].”
• Acute-on-chronic liver failure: consensus recommendations of the Asian Pacific Association for the Study of the Liver (APASL) 2014 (2009, neutral): “Proinflammatory cytokines are believed to mediate hepatic inflammation, apoptosis, and necrosis of liver cells; cholestasis; and fibrosis [32, 45].”
• Non-alcoholic fatty liver disease and its relationship with cardiovascular disease and other extrahepatic diseases (2017, background): “181 There is substantial evidence that activation of the transcription of nuclear factor-κ B (NF-κ B) and down-stream in fl ammatory signalling pathways are involved in metabolic liver in fl ammation and associated hepatic insulin resistance.”
• The fat-derived hormone adiponectin alleviates alcoholic and nonalcoholic fatty liver diseases in mice. (2003, positive): “Many recent studies suggest that several proinflammatory cytokines produced by activated Kupffer cells might be involved in the onset of alcoholic liver disease (4, 5).”
• Kupffer Cells in the Liver (2013, neutral): “TNF-α is primarily produced by monocytes and macrophages; increased TNF-α production is one of the earliest responses of the liver to injury (141).”
• Mouse models in non‐alcoholic fatty liver disease and steatohepatitis research (2006, background): “To identify relevant pathogenic genes and novel models of steatohepatitis, we have collaborated in a random N-ethylN-nitrosourea chemical mutagenesis screen and assayed offspring for insulin resistant, diabetic and NASH phenotypes.”