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Current Molecular Medicine


ISSN (Print): 1566-5240
ISSN (Online): 1875-5666

Mini-Review Article

Critical Role of NFκB in the Pathogenesis of Non-alcoholic Fatty Liver Disease: A Widespread Key Regulator

Author(s): Lorenzo Franceschetti, Francesca Bonomini*, Luigi Fabrizio Rodella and Rita Rezzani

Volume 21, Issue 6, 2021

Published on: 26 October, 2020

Page: [495 - 505] Pages: 11

DOI: 10.2174/1566524020666201026162343

Price: $65


Non-alcoholic fatty liver disease is a chronic metabolic disorder representing the most common cause of chronic liver disease in western civilization and one of the main causes of cirrhosis with a significant impact on all-cause mortality in the most advanced phases. It is characterized by hepatic fat accumulation in the absence of significant ethanol consumption, virus infection or other specific causes of liver disease. Accumulation of fat in liver tissue occurs as a consequence of the imbalance between overconsumption of high-fat diet and increased de novo lipogenesis and decreased lipid disposal. Novel dietary and pharmacological therapies for the prevention of fatty liver disease and the progression to cirrhosis are an actual field of study but still poorly understood. In this perspective, the current review aims to summarise and clarify the transcription factor NFκB effects, which may exert among non-alcoholic fatty liver diseases and their progression. Through extensive previous research, it has become clear that several signaling pathways are involved: metabolic dysregulation (such as free fatty acids increase, adipokine alteration, insulin resistance), oxidative stress and inflammation contribute together in a “vicious circle” to the pathogenesis of non-alcoholic fatty liver diseases. Within this, NFκB signaling is a primary factor in inflammatory reactions and diseases, with important molecular connections between metabolic, oxidative, immune and inflammation systems.

Keywords: Non-alcoholic fatty liver disease, Nuclear factor kappa b, Non-alcoholic steatohepatitis, Hepatic steatosis, inflammation, oxidative stress.

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