Integrating multi-omics data to dissect the genetic driving mechanisms and metabolic regulatory networks of non-alcoholic steatohepatiti

Non-alcoholic fatty liver disease (NAFLD) has become an increasingly common chronic liver disease worldwide, and non-alcoholic steatohepatitis (NASH), as its severe type, is more likely to progress to cirrhosis and even liver cancer. Recently, the role of immune imbalance in the pathogenesis of NAFLD has received much attention, especially the imbalance of Th 1 / Th 2 cell subsets and the abnormal expression of related cytokines. The imbalance between IFN- γand other proinflammatory cytokines secreted by Th 1 cells and anti-inflammatory cytokines such as IL-4 secreted by Th 2 cells can affect hepatic fat metabolism and inflammation. Th 17 cells and their secreted IL-17 aggravate hepatocyte injury by inducing inflammation, while Treg cells and their secreted IL-10 exert anti-inflammatory and immune regulation effects, and the imbalance of both promotes the development of NASH. Integration of multiple omics data, from the genome, transcriptome, proteome and metabolome level, helps to fully resolve the immune imbalance and cytokines abnormalities and NASH genetic driving mechanism and metabolic regulation network, for a deep understanding of NASH pathogenesis, find new biomarkers and the development of targeted treatment strategies.