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实质消退:凝血与肝纤维化形成。

Parenchymal extinction: coagulation and hepatic fibrogenesis.

作者信息

Anstee Quentin M, Wright Mark, Goldin Robert, Thursz Mark R

机构信息

Department of Academic Medicine, St Mary+s Hospital Campus, Imperial College London, 10th Floor, QEQM Building, Praed Street, London W2 1PG, UK.

Department of Hepatology, Southampton General Hospital, Southampton, UK.

出版信息

Clin Liver Dis. 2009 Feb;13(1):117-126. doi: 10.1016/j.cld.2008.09.013.

Abstract

Observations that hepatic inflammation and cirrhosis are associated with the presence of thrombi within the hepatic microvasculature and fibrin-fibrinogen deposition have led to epidemiologic studies showing that carriage of the factor V Leiden mutation, protein C deficiency, and increased expression of factor VIII are associated with rapid progression to cirrhosis in a chronic hepatitis C virus. Additional data suggest that this process may extend more broadly to progression in many forms of chronic liver disease. This article discusses the evidence for a role for coagulation cascade activity in hepatic fibrogenesis and explores the proposed pathogenic mechanisms including the downstream events of thrombin activation. Interference with either the generation of thrombin or its downstream activity may reduce hepatic fibrosis. Also examined are the implications for future therapeutic intervention.

摘要

有观察表明,肝脏炎症和肝硬化与肝微血管内血栓的存在以及纤维蛋白-纤维蛋白原沉积有关,这促使流行病学研究显示,携带凝血因子V莱顿突变、蛋白C缺乏以及凝血因子VIII表达增加与慢性丙型肝炎病毒感染后快速进展为肝硬化有关。更多数据表明,这一过程可能更广泛地延伸至多种形式的慢性肝病进展。本文讨论了凝血级联活动在肝纤维化形成中作用的证据,并探讨了包括凝血酶激活的下游事件在内的推测致病机制。干扰凝血酶的产生或其下游活性可能会减轻肝纤维化。还研究了其对未来治疗干预的影响。

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