Non-alcoholic Steatohepatitis and Hepatocellular Carcinoma are Influenced by Oxidative Stress, Inflammation, and Apoptosis via Activating the AMPKCaspase Axis and JAK/STAT Pathway

The progression of non-alcoholic fatty liver disease (NAFLD) to hepatocellular carcinoma (HCC) and non-alcoholic steatohepatitis (NASH) is looked at in this article. It highlights how inflammation, oxidative stress, apoptosis, and fat accumulation all contribute to this development. Mouse models and patient data are used in the study to explore these pathways. NASH development is linked to the adenosine monophosphate-activated protein kinase (AMPK)-caspase 6 axis, where fibrosis is correlated with caspase 3 and 6 activation. There are preventive benefits against NASH when caspase 3 and 6 are inhibited. Reduction of inflammation and oxidative stress can result in reduced fibrosis and steatosis, which are important contributors to the pathogenesis of NASH. In NASH, the immune system is also essential for managing the inflammatory milieu. The transformation of NAFLD-NASH-HCC is attributed in part to lipid buildup, apoptosis, oxidative stress, inflammation, and the immune system, according to the research. The importance of oxidized phospholipids and the Janus kinase/signal transducers and activators of transcription (JAK/STAT) signaling pathway in the development of HCC and the progression of NASH are also covered. The results offer significant perspectives on possible therapeutic targets, including the JAK/STAT pathway and the AMPK-caspase axis.