期刊名称：Proceedings of the National Academy of Sciences
印刷版ISSN：0027-8424
电子版ISSN：1091-6490
出版年度：1999
卷号：96
期号：5
页码：2345-2349
DOI：10.1073/pnas.96.5.2345
语种：English
出版社：The National Academy of Sciences of the United States of America
摘要：We eliminated type {beta} transforming growth factor (TGF-{beta}) signaling by adenovirus-mediated local expression of a dominant-negative type II TGF-{beta} receptor (AdCAT{beta}-TR) in the liver of rats treated with dimethylnitrosamine, a model of persistent liver fibrosis. In rats that received a single application of AdCAT{beta}-TR via the portal vein, liver fibrosis as assessed by histology and hydroxyproline content was markedly attenuated. All AdCAT{beta}-TR-treated rats remained alive, and their serum levels of hyaluronic acid and transaminases remained at low levels, whereas all the AdCAT{beta}-TR-untreated rats died of liver dysfunction. The results demonstrate that TGF-{beta} does play a central role in liver fibrogenesis and indicate clearly in a persistent fibrosis model that prevention of fibrosis by anti-TGF-{beta} intervention could be therapeutically useful.
