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肝纤维化的小鼠模型可模拟不同病因的人类肝纤维化。

Mouse models of liver fibrosis mimic human liver fibrosis of different etiologies.

作者信息

Martínez Allyson K, Maroni Luca, Marzioni Marco, Ahmed Syed T, Milad Mena, Ray Debolina, Alpini Gianfranco, Glaser Shannon S

机构信息

Department of Internal Medicine, College of Medicine, Texas A&M University Health Science Center, Temple, Texas.

Department of Gastroenterology and Hepatology, Università Politecnica delle Marche, Ancona, Italy.

出版信息

Curr Pathobiol Rep. 2014 Dec 1;2(4):143-153. doi: 10.1007/s40139-014-0050-2.

Abstract

The liver has the amazing capacity to repair itself after injury; however, the same processes that are involved in liver regeneration after acute injury can cause serious consequences during chronic liver injury. In an effort to repair damage, activated hepatic stellate cells trigger a cascade of events that lead to deposition and accumulation of extracellular matrix components causing the progressive replacement of the liver parenchyma by scar tissue, thus resulting in fibrosis. Although fibrosis occurs as a result of many chronic liver diseases, the molecular mechanisms involved depend on the underlying etiology. Since studying liver fibrosis in human subjects is complicated by many factors, mouse models of liver fibrosis that mimic the human conditions fill this void. This review summarizes the general mouse models of liver fibrosis and mouse models that mimic specific human disease conditions that result in liver fibrosis. Additionally, recent progress that has been made in understanding the molecular mechanisms involved in the fibrogenic processes of each of the human disease conditions is highlighted.

摘要

肝脏具有在损伤后自我修复的惊人能力;然而,急性损伤后肝脏再生所涉及的相同过程在慢性肝损伤期间可能会导致严重后果。为了修复损伤,活化的肝星状细胞引发一系列事件,导致细胞外基质成分的沉积和积累,从而使肝实质逐渐被瘢痕组织取代,进而导致纤维化。尽管纤维化是由许多慢性肝病引起的,但其涉及的分子机制取决于潜在病因。由于在人类受试者中研究肝纤维化受到许多因素的影响,模拟人类情况的肝纤维化小鼠模型填补了这一空白。本综述总结了肝纤维化的一般小鼠模型以及模拟导致肝纤维化的特定人类疾病情况的小鼠模型。此外,还强调了在理解每种人类疾病情况的纤维化过程中所涉及的分子机制方面取得的最新进展。

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