Toll-like receptor-4 signaling and Kupffer cells play pivotal roles in the pathogenesis of non-alcoholic steatohepatitis.

By C. Rivera, P. Adegboyega, N. Van Rooijen, Arlene Tagalicud, M. Allman, M. Wallace. Journal of Hepatology, 2007

691 citations recorded by the source corpus.

Subfields: Epidemiology, Hepatology, Immunology

View Paper: https://www.semanticscholar.org/paper/de420fdad07cbd52e3f1b43d2afb09d4442a5129

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. S. Friedman
2. M. Pinzani
3. E. Tsochatzis
4. Gerald I. Shulman
5. M. Yoneda
6. Laura E. Nagy
7. Jeffrey I. Gordon
8. R. Flavell

In Hepatology

1. S. Friedman
2. M. Pinzani
3. Gerald I. Shulman
4. M. Yoneda
5. Laura E. Nagy
6. Y. Sumida
7. Mark A. Barnes
8. M. Pritchard

In Immunology

1. M. Pinzani
2. Gerald I. Shulman
3. Jeffrey I. Gordon
4. R. Flavell
5. S. Friedman
6. S. Eisenbarth
7. Eran Elinav
8. Y. Belkaid

Citations in the corpus

• Inflammasome-mediated dysbiosis regulates progression of NAFLD and obesity (2012, background): “Toll-like receptors (TLR) have a major role in NAFLD pathophysiology due to the liver’s exposure to relatively large amounts of PAMPs derived from the intestine and delivered via the portal circulatio”
• The multiple-hit pathogenesis of non-alcoholic fatty liver disease (NAFLD). (2016, background): “Lipopolysaccharide (LPS) is one of the main toxic bacterial products and it may act, linked to co-receptor CD14, as ligand for TLR with consequent activation of the inflammatory cascade, including stress-activated protein kinases, JNK, p38, interferon regulatory factor 3 and nuclear factor-jB, pathw”
• Mechanisms and disease consequences of nonalcoholic fatty liver disease (2021, background): “Conversely, TLR4 signaling in proinflammatory macrophages in response to endotoxin generates more TGF-b1, a key fibrogenic cytokine (Rivera et al., 2007).”
• Current and future pharmacological therapies for NAFLD/NASH (2017, background): “Inhibition of the TLR4 signaling pathway may provide an effective therapy in the prevention of inflammatory hepatic injury and hepatic fibrosis in NASH patients [75].”
• Kupffer Cells in the Liver (2013, positive): “Just as in mouse models of ALD, mice deficient in TLR4 are protected from high-fat-diet-induced liver injury (115,134).”
• Intestinal microbiota in patients with nonalcoholic fatty liver disease (2013, neutral): “Insulin (pmol/L) 21 (15-61) 33 (15-465) 97 (29-437)”