Hepatic fibrosis

被引：259

作者：

Jiao, Jingjing ^{[1
]}

Friedman, Scott L. ^{[1
]}

Aloman, Costica ^{[1
]}

机构：

[1] Mt Sinai Sch Med, Div Liver Dis, New York, NY 10029 USA

来源：

CURRENT OPINION IN GASTROENTEROLOGY | 2009年 / 25卷 / 03期

关键词：

genetic polymorphism; hepatic stellate cells; liver fibrosis; PDGF; portal fibroblast; TGF-beta; EPITHELIAL-MESENCHYMAL TRANSITION; GROWTH-FACTOR-BETA; MOUSE-LIVER FIBROSIS; DIETARY RAT MODEL; STELLATE CELLS; NONALCOHOLIC STEATOHEPATITIS; TGF-BETA; HEPATOCELLULAR-CARCINOMA; CARBON-TETRACHLORIDE; PORTAL PRESSURE;

D O I：

10.1097/MOG.0b013e3283279668

中图分类号：

R57 [消化系及腹部疾病];

学科分类号：

摘要：

Purpose of review This review will summarize the most significant work that contributed to the understanding of liver fibrosis progression and resolution, which in turn has yielded new areas of therapeutic targeting. Recent findings Liver fibrosis is the result of an imbalance between production and dissolution of extracellular matrix. Stellate cells, portal myofibroblasts, and bone marrow derived cells converge in a complex interaction with hepatocytes and immune cells to provoke scarring in response to liver injury. Uncovering the specific effects of growth factors on these cells, defining the interaction of different cell population during liver fibrosis and characterizing the genetic determinants of fibrosis progression will enable the discovery of new therapeutic approaches. Summary The outcome of improved understanding of liver fibrosis process, especially the regulation and activation of stellate cells, is reflected in the development of new therapeutic strategies, which are validated in animal models.

引用

页码：223 / 229

页数：7

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