Toll‐Like receptor 4 mediates inflammatory signaling by bacterial lipopolysaccharide in human hepatic stellate cells
By Y. Paik, Robert F. Schwabe, R. Bataller, M. Russo, C. Jobin, D. Brenner. Hepatology, 2003
648 citations recorded by the source corpus.
Subfields: Epidemiology, Hepatology
View Paper: https://www.semanticscholar.org/paper/913f590dd6d961c023c50c32ef1f7e503bd4f397
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In Epidemiology
In Hepatology
Citations in the corpus
- TLR4 enhances TGF-β signaling and hepatic fibrosis (2007, background): “We and others have previously shown that activated HSCs express TLR4 and are highly responsive to low concentrations of LP”
- Interaction between microbiota and immunity in health and disease (2020, background): “This results in an upregulation of multiple chemokines and adhesion molecules.(232) Innate immune sensing of gut-derived microbial products by different TLRs, including TLR4, TLR9, TLR5, and their downstream impacts on liver inflammation in the context of NAFLD/NASH have been recently reviewed elsew”
- NF-κB in the liver—linking injury, fibrosis and hepatocellular carcinoma (2011, background): “A wide range of proinflammatory mediators activate NF-κB in HSCs/HMFs, including LPS, TNF, IL-1β, angiotensin II and CD40L”
- Increased intestinal permeability in obese mice: new evidence in the pathogenesis of nonalcoholic steatohepatitis. (2007, background): “Recent evidence, however, has shown that HSCs can directly respond to LPS via a specific receptor complex and contribute to establish and/or enhance endotoxin-mediated liver injury (9, 43).”
- Liver inflammation and fibrosis. (2017, background): “TLR4 activation can lead to ROS signaling, and ROS may modulate signaling downstream of TLR4 via NOX activation.”