Because LOX-1, a receptor for oxidized low-density lipoprotein (ox-LDL), which accumulates on the atherosclerotic vasculature, is suggested to cause oxidative stress-related cell damage [23,24], it is expected that LOX-1 overexpression may further augment organ damage by salt-induced ROS overproduction and cause the progression of NASH. Here, OLR1 is linked to metabolic dysfunction-associated steatohepatitis.