Immunity as Cornerstone of Non-Alcoholic Fatty Liver Disease: The Contribution of Oxidative Stress in the Disease Progression

Non-alcoholic fatty liver disease (NAFLD) is considered the hepatic manifestation of metabolic syndrome and has become the major cause of chronic liver disease, especially in western countries. NAFLD encompasses a wide spectrum of hepatic histological alterations, from simple steatosis to steatohepa...

Full description

Saved in:
Bibliographic Details
Published in:International journal of molecular sciences 2021-01, Vol.22 (1), p.436
Main Authors: Dallio, Marcello, Sangineto, Moris, Romeo, Mario, Villani, Rosanna, Romano, Antonino Davide, Loguercio, Carmelina, Serviddio, Gaetano, Federico, Alessandro
Format: Article
Language:English
Subjects:
Adaptive immunity
Aldehydes
Animals
Cholesterol
Cirrhosis
Cytochrome
Cytokines
Disease Progression
Enzymes
Fatty acids
Fatty liver
Fibrosis
Hepatocellular carcinoma
Humans
Immune system
Immunity (Disease)
Immunity, Cellular - immunology
Inflammation
Insulin
Insulin resistance
Kinases
Lipid metabolism
Lipids
Liver
Liver cancer
Liver cirrhosis
Liver diseases
Macromolecules
Metabolic disorders
Metabolic syndrome
Metabolism
Mitochondria
non-alcoholic fatty liver disease
Non-alcoholic Fatty Liver Disease - immunology
Non-alcoholic Fatty Liver Disease - pathology
Oxidation
Oxidative Stress
Pathogenesis
Proteins
Review
Steatosis
trained immunity
Citations: Items that this one cites
Items that cite this one
Online Access:Get full text
Tags: Add Tag
No Tags, Be the first to tag this record!
Description
Summary:Non-alcoholic fatty liver disease (NAFLD) is considered the hepatic manifestation of metabolic syndrome and has become the major cause of chronic liver disease, especially in western countries. NAFLD encompasses a wide spectrum of hepatic histological alterations, from simple steatosis to steatohepatitis and cirrhosis with a potential development of hepatocellular carcinoma. Non-alcoholic steatohepatitis (NASH) is characterized by lobular inflammation and fibrosis. Several studies reported that insulin resistance, redox unbalance, inflammation, and lipid metabolism dysregulation are involved in NAFLD progression. However, the mechanisms beyond the evolution of simple steatosis to NASH are not clearly understood yet. Recent findings suggest that different oxidized products, such as lipids, cholesterol, aldehydes and other macromolecules could drive the inflammation onset. On the other hand, new evidence indicates innate and adaptive immunity activation as the driving force in establishing liver inflammation and fibrosis. In this review, we discuss how immunity, triggered by oxidative products and promoting in turn oxidative stress in a vicious cycle, fuels NAFLD progression. Furthermore, we explored the emerging importance of immune cell metabolism in determining inflammation, describing the potential application of trained immune discoveries in the NASH pathological context.
ISSN:1422-0067
1661-6596
1422-0067
DOI:10.3390/ijms22010436