TLR4 and metabolic dysfunction-associated steatotic liver disease: For instance, in a non-alcoholic fatty liver disease (NAFLD) model study, it was found that Lcn-2 could trigger the secretion of HMGB1, activate TLR4 signaling pathway, induce NOX-2 expression, increase ROS production, then cause neuronal oxidative damage (55), which increase neuroinflammation.