Immunity as Cornerstone of Non-Alcoholic Fatty Liver Disease: The Contribution of Oxidative Stress in the Disease Progression
Open Access
- 4 January 2021
- journal article
- review article
- Published by MDPI AG in International Journal of Molecular Sciences
- Vol. 22 (1), 436
- https://doi.org/10.3390/ijms22010436
Abstract
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.This publication has 237 references indexed in Scilit:
- ROS play a critical role in the differentiation of alternatively activated macrophages and the occurrence of tumor-associated macrophagesCell Research, 2013
- Regulation of NF-B-Induced Inflammatory Signaling by Lipid Peroxidation-Derived AldehydesOxidative Medicine and Cellular Longevity, 2013
- NF-κB in the liver—linking injury, fibrosis and hepatocellular carcinomaNature Reviews Gastroenterology & Hepatology, 2011
- Crosstalk of reactive oxygen species and NF-κB signalingCell Research, 2010
- A New Population of Myeloid-Derived Suppressor Cells in Hepatocellular Carcinoma Patients Induces CD4+CD25+Foxp3+ T CellsGastroenterology, 2008
- Induction of Immunological Tolerance by Apoptotic Cells Requires Caspase-Dependent Oxidation of High-Mobility Group Box-1 ProteinImmunity, 2008
- Effects of rosiglitazone on the liver histology and mitochondrial function in ob/ob miceJournal of Hepatology, 2007
- Hepatocellular Carcinoma: Epidemiology and Molecular CarcinogenesisGastroenterology, 2007
- Uric acid and anti-TNF antibody improve mitochondrial dysfunction in ob/ob miceJournal of Hepatology, 2006
- Defective hepatic mitochondrial respiratory chain in patients with nonalcoholic steatohepatitisJournal of Hepatology, 2003