Fig. 7From: Thrombospondin 1 enhances systemic inflammation and disease severity in acute-on-chronic liver failureProposed mechanism of THBS1 in HBV-ACLF pathogenesis. A scheme representing the potential role of THBS1 in HBV-ACLF pathophysiology. HBV exacerbation triggers an immune response, and the subsequent hepatic inflammasome activation promotes THBS1 upregulation from hepatocytes and Kupffer cells. THBS1 activates the caspase cascade, mediated by the interaction between THBS1 and its possible receptors and targets (CD36, TGF-β, CD47, integrins) on the surface of the hepatocyte membrane, which generate hepatocellular apoptosis and promote the liver failureBack to article page