Non-parenchymal hepatic cell lipotoxicity and the coordinated progression of non-alcoholic fatty liver disease and atherosclerosis

Current Opinion in Lipidology
Kia M PetersNica M Borradaile

Abstract

Non-alcoholic fatty liver disease (NAFLD) appears to be independently associated with the development of atherosclerosis. The biological mechanisms underlying this association are complex, and likely involve liver-resident cell types other than hepatocytes. Thus, we review recent evidence that non-parenchymal hepatic cell responses to lipid excess contribute to the pathogenesis of both NAFLD and atherosclerosis. Significant independent associations between NAFLD and atherosclerosis have been identified through cross-sectional studies and meta-analyses. Mechanistic studies in cell cultures and in rodent models suggest that liver-resident macrophages, activated hepatic stellate cells (HSC) and liver sinusoidal endothelial cells (LSEC) mount lipotoxic responses under NAFLD conditions which can contribute to the progression of both NAFLD and atherosclerosis. Non-parenchymal hepatic cell types exhibit some similarity in their responses to lipid excess, and in their pathogenic mechanisms, which likely contribute to the coordinated progression of NAFLD and atherosclerosis. In response to lipotoxic conditions, macrophages, Kupffer cells and HSC initiate robust inflammatory responses, whereas LSEC generate excess reactive oxygen species...Continue Reading

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Citations

Jun 4, 2020·Hepatology Communications·Conor O'DwyerMorgan D Fullerton
Apr 4, 2021·International Journal of Molecular Sciences·Daniel Lam-SidunNica M Borradaile
Feb 24, 2019·Journal of Hepatology·Adel Hammoutene, Pierre-Emmanuel Rautou
Sep 26, 2020·Pharmacological Research : the Official Journal of the Italian Pharmacological Society·Rachel B WilsonNica M Borradaile

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