Non-alcoholic fatty liver disease (NAFLD) or metabolic dysfunction-associated fatty liver disease (MAFLD) becomes the most common chronic liver disease, affecting a quarter of the world population. A progressive form of NAFLD/MAFLD is non-alcoholic steatohepatitis (NASH) with the progression of liver inflammation and varying degrees of fibrosis, which may lead to liver cirrhosis and cancer, such as hepatocellular carcinoma (HCC). The prevalence of NASH is increasing due to a raising trend of obesity, diabetes, and metabolic related disease. However, there is no currently approved treatment for NAFLD/MAFLD. Infiltrated circulating immune cells or bone marrow-derived immune cells and liver resident immune cells such as macrophages and monocytes play important roles in the pathogenesis of these chronic liver diseases. Activation of molecular signaling pathways involved in liver inflammation, cell death, and fibrosis accounts for the progression of NAFLD/MAFLD to NASH, promoting cancer development and progression. Thus, it is essential to understand the underlying cellular and molecular mechanisms involved in the pathogenesis of NAFLD or MAFLD, and their progression to the end-stage of liver disease. In addition, regulating these targets could prevent or reverse the disease progression. This special issue focuses on the "Cellular and molecular targets for NAFLD or MAFLD treatments and their functions in liver fibrosis, cirrhosis, and cancer". Here, we aim to provide a comprehensive understanding of the latest research and clinical findings in this field and provide potential therapeutic targets for NASH and liver cancer, as well as future research directions. We are collecting original research and review articles of basic and clinical studies from experts in the field to enhance our current understanding of the pathogenesis of NAFLD/MAFLD, NASH, and their mediated liver cancer development.

Keywords: NAFLD, MAFLD, NASH, fibrosis, liver cancer, cellular and molecular mechanisms, targets, treatments