WU Yarong, ZHANG Yongqiang, ZHENG Ying, WANG Caihong. Advances in Mechanisms of Portal Vein Thrombosis in Liver Cirrhosis[J]. Medical Journal of Peking Union Medical College Hospital, 2025, 16(2): 439-447. DOI: 10.12290/xhyxzz.2024-0924
Citation: WU Yarong, ZHANG Yongqiang, ZHENG Ying, WANG Caihong. Advances in Mechanisms of Portal Vein Thrombosis in Liver Cirrhosis[J]. Medical Journal of Peking Union Medical College Hospital, 2025, 16(2): 439-447. DOI: 10.12290/xhyxzz.2024-0924

Advances in Mechanisms of Portal Vein Thrombosis in Liver Cirrhosis

Funds: 

Gansu Province Health Industry Research Program GSWSKY2023-303

Lanzhou Science and Technology Plan Project 2023-4-1

G Program of The 940th Hospital of PLA Joint Logistic Support Force 2024-G2-4

More Information
  • Corresponding author:

    ZHENG Ying, E-mail: 13919934061@139.com

  • Received Date: November 15, 2024
  • Accepted Date: December 26, 2024
  • Available Online: January 17, 2025
  • Publish Date: January 16, 2025
  • Issue Publish Date: March 29, 2025
  • Portal vein thrombosis (PVT) is one of the most common complications of liver cirrhosis. The formation of PVT can increase the mortality rate of cirrhotic patients and adversely affect the successful implementation and prognosis of liver transplantation. A hypercoagulable state is a unique mechanism underlying PVT formation in cirrhotic patients. In recent years, the pathogenesis of PVT has gradually been elucidated, with specific mechanisms including the following aspects: systemic and local inflammatory responses lead to vascular endothelial cell dysfunction, thereby promoting the activation of the coagulation system; abnormal activation of the monocyte-macrophage system exacerbates local inflammation, enhancing platelet adhesion and aggregation, and facilitating thrombus formation; an imbalance between the coagulation and fibrinolytic systems results in a sustained hypercoagulable state; and intestinal microbiota dysbiosis induces inflammation and metabolic disturbances, thereby increasing the risk of PVT. This article summarizes the latest research progress on these key mechanisms and their interactions, providing new insights into the molecular and cellular mechanisms of PVT. It also offers directions for the early diagnosis of PVT and the exploration of novel intervention strategies in the future.

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