摘要
肝纤维化是肝脏对一系列慢性刺激的损伤修复反应,以细胞外基质的过度沉积为主要特征。许多研究证明人肝星状细胞(hepatic stellate cells,HSCs)的活化与增殖是肝纤维化形成的中心环节。因此,肝星状细胞激活机制及抑制活化途径的研究和发现成为防治肝纤维化的关键。目前,国际上肝纤维化药物研发的思路之一是从肝纤维化发生的机制,即肝星状细胞激活机制中寻找分子靶点。近年来,对各种使肝星状细胞活化的信号通路及相关抑制机制的研究取得了一些进展,但由于肝星状细胞活化是多条信号通路相互协调的结果,其复杂性、未知性造成了阻断方式的特异性、多样性,使该研究还仅限于实验室阶段,要想应用于临床还需要大量实验证明。该文就最新发现的肝星状细胞激活和抑制及相关分子机制作一综述。
Liver fibrosis is the excessive accumulation of extracellular matrix （ECM） proteins resulting from chronic liver damage. Cirrhosis is the end-stage consequence of fibrosis of the hepatic parenchyma. If liver fibrosis can be detected and treated early, cirrhosis can be prevented. During the past 20 years, much research has proved that the activation and proliferation of hepatic stellate cells （HSCs） play a pivotal role in liver fibrogenesis. One of the current international thinkings on developing anti-fibrotic drugs is to find molecular targets from the mechanism of liver fibrosis, especially HSCs activation mechanism. As a result of the ＂communication＂ of multiple signal pathways, HSCs activation mechanisms and the related inhibition mechanisms are especially complicated and varied. In recent years, some progress has been made on the related mechanisms of HSCs and some molecular mechanisms are still unknown. The main purpose of this paper is to summarize updated activation and inhibition of human HSCs and the related molecular mechanisms.
出处
《中国细胞生物学学报》
CAS
CSCD
2011年第10期1127-1136,共10页
Chinese Journal of Cell Biology
基金
国家自然科学基金(No.30870549)
教育部高等学校博士学科点专项科研基金(No.200806970018
No.20106101110012)资助项目~~
关键词
肝纤维化
肝星状细胞
激活
抑制活化
分子机制
liver fibrosis
hepatic stellate cells
activation
inhibition
molecular mechanism
