TBCE and portal hypertension: LSEC dysfunction is sustained by a continuous and intricate interplay between different cell types and molecules; hepatocytes, HSCs, myofibroblasts, neutrophils, KCs, and other activated leukocytes, but also BAs and endotoxin acting on the other side of GVB all play a pivotal role in favoring fibrosis progression through the constitution of a pro-inflammatory and thrombogenic milieu, invariably characterized by the increase in ROS production and shear stress that leads to increased IVHR up to portal hypertension occurrence.