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Abstract Details
Infections at the nexus of metabolic-associated fatty liver disease
Arch Toxicol. 2021 May 24;1-19. doi: 10.1007/s00204-021-03069-1.Online ahead of print.
Joost Boeckmans12, Matthias Rombaut3, Thomas Demuyser45, Baptist Declerck4, Denis Piérard4, Vera Rogiers3, Joery De Kock3, Luc Waumans6, Koen Magerman67, Reinoud Cartuyvels6, Jean-Luc Rummens6, Robim M Rodrigues#8, Tamara Vanhaecke#3
Author information
1Department of In Vitro Toxicology and Dermato-Cosmetology, Faculty of Medicine and Pharmacy, Vrije Universiteit Brussel, Laarbeeklaan 103, 1090, Brussels, Belgium. Joost.Boeckmans@vub.be.
3Department of In Vitro Toxicology and Dermato-Cosmetology, Faculty of Medicine and Pharmacy, Vrije Universiteit Brussel, Laarbeeklaan 103, 1090, Brussels, Belgium.
7Department of Immunology and Infection, Hasselt University, Martelarenlaan 42, 3500, Hasselt, Belgium.
8Department of In Vitro Toxicology and Dermato-Cosmetology, Faculty of Medicine and Pharmacy, Vrije Universiteit Brussel, Laarbeeklaan 103, 1090, Brussels, Belgium. Robim.Marcelino.Rodrigues@vub.be.
#Contributed equally.
Abstract
Metabolic-associated fatty liver disease (MAFLD) is a chronic liver disease that affects about a quarter of the world population. MAFLD encompasses different disease stadia ranging from isolated liver steatosis to non-alcoholic steatohepatitis (NASH), fibrosis, cirrhosis and hepatocellular carcinoma. Although MAFLD is considered as the hepatic manifestation of the metabolic syndrome, multiple concomitant disease-potentiating factors can accelerate disease progression. Among these risk factors are diet, lifestyle, genetic traits, intake of steatogenic drugs, male gender and particular infections. Although infections often outweigh the development of fatty liver disease, pre-existing MAFLD could be triggered to progress towards more severe disease stadia. These combined disease cases might be underreported because of the high prevalence of both MAFLD and infectious diseases that can promote or exacerbate fatty liver disease development. In this review, we portray the molecular and cellular mechanisms by which the most relevant viral, bacterial and parasitic infections influence the progression of fatty liver disease and steatohepatitis. We focus in particular on how infectious diseases, including coronavirus disease-19, hepatitis C, acquired immunodeficiency syndrome, peptic ulcer and periodontitis, exacerbate MAFLD. We specifically underscore the synergistic effects of these infections with other MAFLD-promoting factors.