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Abstract Details
Fibrogenic Pathways in Metabolic Dysfunction Associated Fatty Liver Disease (MAFLD)
Int J Mol Sci. 2022 Jun 23;23(13):6996. doi: 10.3390/ijms23136996.
1Institute for Clinical Chemistry and Laboratory Medicine, University Hospital and Faculty of Medicine, Technische Universität Dresden, 01307 Dresden, Germany.
2Department of Internal Medicine I, University Hospital and Faculty of Medicine, Technische Universität Dresden, 01307 Dresden, Germany.
3Department of Hepatology & Gastroenterology, Campus Virchow-Klinikum and Campus Charité Mitte, Charité Universitätsmedizin Berlin, 13353 Berlin, Germany.
4Paul Langerhans Institute Dresden, Helmholtz Zentrum München, University Hospital and Faculty of Medicine, Technische Universität Dresden, 01307 Dresden, Germany.
5German Center for Diabetes Research, 85764 Neuherberg, Germany.
Abstract
The prevalence of nonalcoholic fatty liver disease (NAFLD), recently also re-defined as metabolic dysfunction associated fatty liver disease (MAFLD), is rapidly increasing, affecting ~25% of the world population. MALFD/NAFLD represents a spectrum of liver pathologies including the more benign hepatic steatosis and the more advanced non-alcoholic steatohepatitis (NASH). NASH is associated with enhanced risk for liver fibrosis and progression to cirrhosis and hepatocellular carcinoma. Hepatic stellate cells (HSC) activation underlies NASH-related fibrosis. Here, we discuss the profibrogenic pathways, which lead to HSC activation and fibrogenesis, with a particular focus on the intercellular hepatocyte-HSC and macrophage-HSC crosstalk.