Study on mechanisms of comorbidity between hepatocellular steatosis and atherosclerosis based on metabolomics and network pharmacology.

The abnormal lipid metabolism and inflammatory response are the distinctive features of the co-morbid model of AS and NAFLD, which were interreacted with each other. Hepatocyte steatosis causes mitochondrial damage, which leads to mitochondrial dysfunction, increased reactive oxygen species and activation of the macrophage inflammatory response, resulting in the acceleration of AS development.