TLR4 enhances TGF-beta signaling and hepatic fibrosis.

By E. Seki, S. de Minicis, Christoph H Osterreicher, J. Kluwe, Y. Osawa, D. Brenner, Robert F. Schwabe. Nature Medicine, 2007

819 citations recorded by the source corpus.

View Paper: https://www.semanticscholar.org/paper/e2dded0cce803fe6d1d860f1a32ae48099245e7e

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1. F. Tacke
2. P. Angeli
3. M. Pinzani
4. R. Jalan
5. E. Seki
6. Christian Trautwein
7. T. Kisseleva
8. M. Bernardi

Citations in the corpus

• Myofibroblasts revert to an inactive phenotype during regression of liver fibrosis (2012, methodology): “The contribution of aHSCs to liver myofibroblasts in CCl4-treated Col-GFP mice was determined using flow cytometry of the isolated nonparenchymal liver cell fraction, which contains aHSCs/myofibroblasts, inflammatory cells, and endothelial cells (8).”
• Liver sinusoidal endothelial cells: Physiology and role in liver diseases. (2017, background): “This limitation can be overcome by performing a transplantation of wild type bone marrow together with a clodronate mediated Kupffer cell depletion [73].”
• Bacterial infections in cirrhosis: a position statement based on the EASL Special Conference 2013. (2014, background): “Reducing the intestinal bacterial burden with antibiotics ameliorates experimental liver disease [38,39] and, decreases the liver disease severity [40,41] and infectious complications in patients with advanced cirrhosis [42].”
• Hepatic fibrosis: Concept to treatment. (2015, background): “An example is the activation of toll-like receptor 4 (TLR4) that leads to repression of the activin membrane bound inhibitor BAMBI, which further enhances TGFb-dependent HSC activation [6,7].”
• Promotion of Hepatocellular Carcinoma by the Intestinal Microbiota and TLR4 (2012, methodology): “, 2004) and reduces systemic LPS levels (Seki et al., 2007).”
• Microbiota in health and diseases (2022, background): “described that, upon LPS binding, TLR4 upregulates chemokine secretion and downregulates TGF-β pseudoreceptor Bambi to enhance TGF-β signaling pathway.(327) The study also suggested that the effect of LPS is mediated by MyD88-NF-κB-dependent pathway, as MyD88deficient mice had decreased hepatic fibr”
• Macrophage heterogeneity in liver injury and fibrosis. (2014, background): “Target Inhibition of (Ly-6C+) inflammatory Possible approach (selected from experimental models) • Pharmacological antagonism of CCL2 (MCP-1) small using inhibitory RNA molecules (socalled Spiegelmers) [16] • Pharmaceutical inhibition of CCR2 [24] • Intestinal decontamination by antibiotics, leading”
• Micro‐RNA profiling reveals a role for miR‐29 in human and murine liver fibrosis (2011, result): “In line with our findings, it was previously shown that LPS stimulation alone does not lead to increased collagen production in HSCs.24 It is possible that miR-29–dependent effects on their target mRNAs require a previous strong induction of the respective extracellular matrix genes by TGF-b.”
• Hepatic Inflammation and Fibrosis: Functional Links and Key Pathways (2015, background): “Mediators that increase NF-jB and survival in HSCs appear to be largely derived from KCs, such as IL-1b and TNF-a,(6) but also include LPS and its receptor, TLR4.(14) In addition, NF-jB activation triggers secretion of chemokines by HSCs (promoting recruitment and interaction with inflammatory cells”
• Gut microbiome based metagenomic signature for non-invasive detection of advanced fibrosis in human nonalcoholic fatty liver disease (2017, unknown): “(Affo et al., 2014; Bai et al., 2016; Liu et al., 2016; Seki et al., 2007) Lelouvier and colleagues have also recently reported that Proteobacteria are increased in morbidly obese individuals undergoing bariatric surgery who have presence of fibrosis(Lelouvier et al., 2016).”