期刊
GASTROENTEROLOGIE CLINIQUE ET BIOLOGIQUE
卷 33, 期 10-11, 页码 949-957出版社
MASSON EDITEUR
DOI: 10.1016/j.gcb.2009.07.021
关键词
-
资金
- German Research Foundation (DFG)
- US National Institutes of Health (NIH)
- European Association for the Study of the Liver (EASL)
We have made striking progress in our understanding of the biochemistry and cell biology that underlies liver fibrosis and cirrhosis, including the development of strategies and agents to prevent and reverse fibrosis and incipient cirrhosis. However, translation of this knowledge into clinical practice has been hampered by the limitation of many in vitro and in vivo models to confirm mechanisms and to test antifibrotic agents, as well as the lack of sensitive methodologies to quantify the degree of liver fibrosis and the dynamics of fibrosis progression or reversal. Furthermore, white cirrhosis and subsequent decompensation are accepted hard clinical end-points, fibrosis and fibrosis progression alone are merely plausible surrogates for future clinical. deterioration. This review focuses on basic mechanisms that underlay liver fibrosis progression and reversal and optimized strategies for preclinical antifibrotic drug development and validation. Therapies include several drugs that are of proven safety for other indications, agents that interfere with major fibrogenic or fibrolytic mechanisms, targeted drug delivery to the fibrogenic liver cells, and their potential combinations with hepatocyte or stem cell replenishment. (C) 2009 Elsevier Masson SAS. All rights reserved.
作者
我是这篇论文的作者
点击您的名字以认领此论文并将其添加到您的个人资料中。
推荐
暂无数据