Background & Aims: Growing evidence supports a role of gut-derived metabolites in nonalcoholic fatty liver disease (NAFLD), but the relation of endotoxin levels with gut permeability and NAFLD stage remains unclear. This systematic review with meta-analysis aims to provide further insights.
Methods: PubMed, Embase, and Cochrane Library were searched for studies published until January 2022 assessing blood endotoxins in patients with NAFLD.
The Nrf2 signaling pathway prevents cancer initiation, but genetic mutations that activate this pathway are found in various types of cancer. The molecular mechanisms underlying this Janus-headed character are still not understood. Here, we show that sustained Nrf2 activation induces proliferation and dedifferentiation of a Wnt-responsive perivenular hepatic progenitor cell population, transforming them into metastatic cancer cells.
View Article and Find Full Text PDFHepatic steatosis and chronic hepatocyte damage ultimately lead to liver fibrosis. Key pathophysiological steps are the activation and transdifferentiation of hepatic stellate cells. We assessed the interplay between hepatocytes and hepatic stellate cells under normal and steatotic conditions.
View Article and Find Full Text PDFHepatic dendritic cells represent a unique and multifaceted subset of antigen-presenting leukocytes that orchestrate specified immune responses in the liver. They are constantly exposed to antigens and signals derived not only from the hepatic microenvironment and the systemic circulation but also from the portal vein draining the gut and conveying food antigens as well as microbial compounds. Modulated by these various factors they shape intrahepatic immune responses during acute and chronic liver diseases, hepatocellular carcinoma and allograft tolerance as well as systemic responses to gut-derived components.
View Article and Find Full Text PDFTwo polymorphisms in the promoter region of macrophage migration inhibitory factor (MIF) - rs755622 and rs5844572 - exhibit prognostic relevance in inflammatory diseases. The aim of this study was to investigate a correlation between these MIF promoter polymorphisms and the severity of hepatitis C virus (HCV)-induced liver fibrosis. Our analysis included two independent patient cohorts with HCV-induced liver fibrosis (504 and 443 patients, respectively).
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