肝脏相关出凝血功能障碍的机制与处理研究进展OA

Liver-related coagulation dysfunction is commonly observed in liver cirrhosis,hepatocellular carcinoma,sepsis-associated liver injury,and post-hepatectomy states.The underlying pathology is a remodeling and dysregulation of the dynamic equilibrium among procoagulant,anticoagulant,and fibrinolytic systems,often manifesting as coexisting bleeding and thrombosis.The traditional coagulation cascade model and routine coagulation tests primarily focus on changes in coagulation factor levels,which fail to fully capture the multicellular synergistic regulation and dynamic hemostatic status within the hepatic microenvironment.Recent advances in the cell-based coagulation model,immunothrombosis theory,and hepatic sinusoidal biology multicellular interaction research have revealed that liver hemostasis regulation is a dynamic network involving hepatocytes,liver sinusoidal endothelial cells,Kupffer cells and inflammatory signals.Under physiological conditions,liver is responsible for the synthesis,supply,and clearance of coagulation factors.Under pathological conditions,this network undergoes remodeling,characterized by disrupted hepatic sinusoidal multicellular interactions and an imbalance in coagulation factor synthesis-clearance homeostasis.Further perspectives should reconceptualize liver hemostatic regulation from a multicellular network and dynamic systems viewpoint,integrating molecular biology techniques with dynamic functional monitoring to establish more precise assessment and intervention strategies.