While NOX4 contributes to fibrosis development directly, by inducing HSC activation, and indirectly, by triggering apoptotic cell death in hepatocytes [55,88], increased NOX1 expression in LSEC isolated from high-fat-diet-fed mice has been associated with enhanced ROS and peroxynitrite-induced hepatocellular injury and impaired hepatic microcirculation, thus accelerating cell death and NASH progression [62]. Here, NOX1 is linked to metabolic dysfunction-associated steatohepatitis.