Nonalcoholic fatty liver disease (NAFLD), recently re-named to metabolic dysfunction associated fatty liver disease (MAFLD) is a major health problem, as it affects ∼25% of the population globally and is a major cause of hepatic cirrhosis and thereby liver failure, as well as hepatocellular carcinoma (HCC). MALFD comprises a broad range of pathological conditions in the liver, including simple fat accumulation (steatosis) and the more progressive non-alcoholic steatohepatitis (NASH) that can lead to fibrosis development. Cells of innate immunity, and particularly macrophages, comprising the liver resident Kupffer cells and the recruited monocyte-derived macrophages play complex roles in NASH-related inflammation and disease progression to fibrosis. Here, we discuss the recent developments with regards to the function of liver macrophage subpopulations during MAFLD development and progression. Abstract figure legend: Liver macrophages in metabolic dysfunction associated fatty liver disease. Different liver macrophage subpopulations, including Kupffer cells (KC) and monocyte-derived macrophages (MoMf), play multiple roles in the pathogenesis and progression of metabolic dysfunction associated fatty liver disease (MAFLD). This article is protected by copyright. All rights reserved.
Institut(e)Institute for Pancreatic Beta Cell Research (IPI)
FörderungenDeutsche Forschungsgemeinschaft Sonderzuweisung zur Unterstuetzung profilbestimmender Struktureinheiten 2021' by the SMWK(Saxon State Ministry of Science, Culture and Tourism) DEEP-HCC project of the LiSyM-cancer program of the BMBF (Federal Ministry of Education and Research)