综述

肝硬化失代偿期门静脉高压症病理生理及分子机制改变的研究进展

  • 樊强 ,
  • 吴广博 ,
  • 赵劲博 ,
  • 郑磊 ,
  • 罗蒙
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  • 上海交通大学医学院附属第九人民医院普外科,上海 201999
樊 强(1984—),男,博士生;电子信箱:13472665251@163.com
罗 蒙,电子信箱:luosh9hospital@sina.com

收稿日期: 2023-10-23

  录用日期: 2023-12-08

  网络出版日期: 2024-03-28

基金资助

国家自然科学基金青年项目(82100639);国家自然科学基金面上项目(81970526);上海交通大学医学院附属第九人民医院基础研究助推计划种子基金(JYZZ162)

Research progress in pathophysiological and molecular mechanism changes during decompensated phase of portal hypertension in liver cirrhosis

  • Qiang FAN ,
  • Guangbo WU ,
  • Jinbo ZHAO ,
  • Lei ZHENG ,
  • Meng LUO
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  • Department of General Surgery, Shanghai Ninth People's hospital, Shanghai Jiao Tong University School of Medicine, Shanghai 201999, China
LUO Meng, E-mail: luosh9hospital@sina.com.

Received date: 2023-10-23

  Accepted date: 2023-12-08

  Online published: 2024-03-28

Supported by

Youth Project of the National Natural Science Foundation of China(82100639);General Project of the National Natural Science Foundation of China(81970526);Fundamental Research Program Funding of Shanghai Ninth People′s Hospital, Shanghai Jiao Tong University School of Medicine(JYZZ162)

摘要

多种病因引起的肝硬化可导致门静脉高压症。处于肝硬化失代偿期的门静脉高压症患者预后显著不佳。由多种并发症引起的患者内环境紊乱通常会演变为肝内外器官功能衰竭。对于由不同病因引起的肝硬化,在早期尚可应用一些缓解药物,但目前关于肝硬化失代偿期门静脉高压症患者疾病进展的机制尚不明确,也缺乏针对疾病进展的有效治疗方案。因此,揭示肝硬化失代偿期门静脉高压症的病理生理机制,以及寻找治疗疾病的有效药物靶点,成为当前研究的重点。该文总结了在肝硬化失代偿期肝内外器官衰竭的病理生理改变,简述了肝内血管阻力、门静脉系统、心血管系统及炎症介质等相关细胞分子调节机制。通过全面分析肝硬化失代偿期门静脉高压症的病理生理发展进程,能够更好地理解引起病情恶化或缓解的潜在细胞分子机制,有助于提高疾病的诊断准确性和对疾病分期的正确把握。此外,发现阻断疾病恶化的药物治疗靶点将指导临床工作者更好地应对难治性门静脉高压症,改善患者预后。

本文引用格式

樊强 , 吴广博 , 赵劲博 , 郑磊 , 罗蒙 . 肝硬化失代偿期门静脉高压症病理生理及分子机制改变的研究进展[J]. 上海交通大学学报(医学版), 2024 , 44(3) : 379 -384 . DOI: 10.3969/j.issn.1674-8115.2024.03.011

Abstract

Cirrhosis caused by multiple etiologies can lead to portal hypertension. The prognosis of patients with portal hypertension in decompensated cirrhosis is significantly poor. Disorders in the patient′s internal environment caused by various complications often evolve into organ failure both inside and outside the liver. For cirrhosis caused by different etiologies, there are still some relief drugs used in the early stages, but the mechanism of disease progression in patients with decompensated cirrhosis and portal hypertension is currently unclear, and there is a lack of effective treatment plans for disease progression. Therefore, revealing the pathophysiological mechanisms of decompensated cirrhosis with portal hypertension and seeking effective drug targets for treating this disease have become the focus of current research. This article summarizes the pathological and physiological changes of intrahepatic and extrahepatic organ failure during the decompensated phase of liver cirrhosis, and briefly describes the cellular and molecular regulatory mechanisms related to intrahepatic vascular resistance, portal system, cardiovascular system, and inflammatory mediators. By comprehensively analyzing the pathological and physiological development process of decompensated cirrhosis with portal hypertension, the potential cellular and molecular mechanisms that cause disease deterioration or remission can be better understood, which can help improve the accuracy of disease diagnosis and the correct grasp of disease staging. In addition, identifying drug treatment targets to block the progression of the disease will guide clinical staff to better cope with refractory portal hypertension, and even improve the prognosis of patients.

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