肝硬化门静脉血栓形成机制研究进展

Advances in molecular and cellular mechanisms of portal vein thrombosis in liver cirrhosis

  • 摘要: 门静脉血栓(portal vein thrombosis,PVT)是肝硬化最常见并发症之一。PVT的形成增加了肝硬化患者的病死率,影响肝移植的顺利实施和术后预后。高凝状态是肝硬化患者中PVT的特殊发生机制。近年来,PVT的多维机制被逐渐揭示,系统性和局部炎症反应的发生,损伤血管内皮细胞功能,促进凝血系统的活化;单核-巨噬细胞系统异常活化加剧局部炎症,增强血小板的粘附和聚集,推动血栓形成;凝血与纤溶系统失衡导致持续的高凝状态;肠道菌群失调,放大了炎症和代谢紊乱,加重了PVT的发生风险。本文通过综述上述关键机制及其相互作用的最新研究进展,为深入揭示PVT的分子与细胞机制提供新视角,同时为PVT的早期诊断和探索新型干预策略指明了未来方向。

     

    Abstract: Portal vein thrombosis (PVT) is one of the most common complications of liver cirrhosis. Its formation increases the mortality of patients with liver cirrhosis and affects the smooth implementation of liver transplantation and postoperative prognosis. Hypercoagulable state is a special mechanism of PVT in patients with liver cirrhosis. In recent years, the multi-dimensional mechanism of PVT has been gradually revealed, and the occurrence of systemic and local inflammatory reactions has damaged the function of vascular endothelial cells and promoted the activation of coagulation system. Abnormal activation of monocyte-macrophage system aggravates local inflammation, enhances platelet adhesion and aggregation, and promotes thrombosis. The imbalance of coagulation and fibrinolysis system leads to a continuous hypercoagulable state ; intestinal dysbacteriosis amplifies inflammation and metabolic disorders, increasing the risk of PVT. By reviewing the latest research progress of the above key mechanisms and their interactions, this paper provides a new perspective for further revealing the molecular and cellular mechanisms of PVT, and points out the future direction for the early diagnosis of PVT and the exploration of new intervention strategies.

     

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