Key result
Oxidative stress drives NAFLD progression to fibrosis and cirrhosis by promoting inflammation and immune activation.
Why the study?
Oxidative stress plays a key role in the development and progression of NAFLD/NASH, but its contribution to hepatic inflammation and disease evolution requires reappraisal.
This review highlights the mechanistic role of oxidative stress in driving hepatic inflammation and the progression of NAFLD to NASH and cirrhosis.
Supports oxidative stress as therapeutic target in NAFLD; leaves open whether antioxidants alter fibrosis progression in trials.
In the last decade, non-alcoholic fatty liver disease (NAFLD) and particularly its evolution to nonalcoholic steatohepatitis (NASH) have become a leading cause of chronic liver disease and cirrhosis as well as an important risk factor for hepatocellular carcinoma. Oxidative stress is a common feature of NAFLD/NASH and plays a key role in the complex of metabolic and cellular derangements that are involved in the development of liver steatosis, as well as in the transition to steatohepatitis. This review deals with the contribution of oxidative stress in promoting hepatic inflammation which represents a key factor in NAFLD evolution to liver fibrosis/cirrhosis. We discuss in detail recent data involving oxidative stress products as triggers for hepatic innate immunity and as a source of antigens implicated in sustaining lymphocyte-mediated adaptive immune responses. Attention is also paid to emerging evidence linking oxidative stress and extra-hepatic complications of NAFLD/NASH.
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Emanuele Albano (2022) conducted a review in Nonalcoholic fatty liver disease (NAFLD) and nonalcoholic steatohepatitis (NASH). Oxidative stress was evaluated. Oxidative stress promotes hepatic inflammation, triggering innate immunity and sustaining adaptive immune responses, which drives the evolution of NAFLD to liver fibrosis and cirrhosis.
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