Subramanian Pallavi, Chavakis Triantafyllos
Institute for Clinical Chemistry and Laboratory Medicine, University Hospital and Faculty of Medicine, Technische Universität Dresden, Dresden, Germany.
Paul Langerhans Institute Dresden, Helmholtz Zentrum München, University Hospital and Faculty of Medicine, Technische Universität Dresden, Dresden, Germany.
J Physiol. 2023 Apr;601(7):1159-1171. doi: 10.1113/JP283820. Epub 2023 Mar 11.
Non-alcoholic fatty liver disease (NAFLD), recently also defined as 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. 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.
非酒精性脂肪性肝病(NAFLD),最近也被定义为代谢功能障碍相关脂肪性肝病(MAFLD),是一个主要的健康问题,因为它影响全球约25%的人口,是肝硬化进而肝衰竭以及肝细胞癌的主要原因。MAFLD包括肝脏中广泛的病理状况,包括单纯脂肪堆积(脂肪变性)以及更进展性的非酒精性脂肪性肝炎(NASH),后者可导致纤维化发展。固有免疫细胞,特别是巨噬细胞,包括肝脏驻留的库普弗细胞和募集的单核细胞衍生巨噬细胞,在NASH相关炎症和疾病进展为纤维化过程中发挥复杂作用。在此,我们讨论了在MAFLD发生和发展过程中肝脏巨噬细胞亚群功能的最新进展。