ACACA and steatosis: revealed that combined exposure to PM2.5 and HFD significantly increased ROS levels to upregulate lipogenesis-related genes such as SREBP1, liver X receptor α (LXRα), SCD1, fatty acid synthase (FAS), and acetyl-CoA carboxylase 1 (ACC1) and the subsequent upregulate miR-155 expression caused the downregulation of peroxisome proliferator-activated receptor γ (PPARγ), ultimately promoting hepatic lipid metabolism disorders and steatosis [9].