TLR4 enhances TGF-β signaling and hepatic fibrosis

By E. Seki, S. Minicis, C. Österreicher, J. Kluwe, Y. Osawa, D. Brenner, Robert F. Schwabe. Nature Medicine, 2007

1,265 citations recorded by the source corpus.

Subfields: Epidemiology, Hepatology, Nutrition and Dietetics

View Paper: https://www.semanticscholar.org/paper/a17f55a094223f86815369034eb4b91d64f63d3d

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Citations in the corpus

Liver inflammation and fibrosis. (2017, background): “TLR4 activation can lead to ROS signaling, and ROS may modulate signaling downstream of TLR4 via NOX activation.”
The endocannabinoid system links gut microbiota to adipogenesis (2010, background): “…(Cani et al, 2007b, 2009; Martin et al, 2008) and a high-fat diet (HFD) (Cani et al, 2007a, 2008)) and drastic models (e.g. antibiotic treatment (Seki et al, 2007; Cani et al, 2008; Membrez et al, 2008) and germ-free mice (Backhed et al, 2004)) of gut microbiota modulation, in addition to mice…”
The Role of Cancer-Associated Fibroblasts and Fibrosis in Liver Cancer (2016, background): “Likewise, activation of TLR4 by gut-derived lipopolysaccharide (LPS) promotes not only the development of liver fibrosis (69) but also of HCC (70), with HSC-derived cytokines such as epiregulin providing possible links between these two (70).”
Liver fibrosis: Pathophysiology, pathogenetic targets and clinical issues. (2019, background): “In addition, as for ROS and other oxidative stress mediators (Novo and Parola, 2008), acetaldehyde can directly activate HSC/MFs and to stimulate expression of collagen type I (Mello et al., 2008).”
Interactions between gut microbiota and host metabolism predisposing to obesity and diabetes. (2011, background): “Interactions with such molecules further promote a widespread inflammatory response in cells expressing TLR4: gut immune cells, adipocytes, endothelial cells, tissue macrophages, hepatocytes, and hepatic Kupffer and stellate cells (70, 71).”
NF-κB in the liver—linking injury, fibrosis and hepatocellular carcinoma (2011, background): “(3) The NF-κB activation in activated hepatic stellate cells is mediated by LPS, mediators released from Kupffer cells (such as IL-1β and TNF) and AngII, which is released and acts on HSCs in an autocrine manner.”