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FoxL在TGF-β/Smad通路中对肝星状细胞活化的影响 被引量:1

Role of forkhead L2 in transforming growth factorbeta/Smad signaling pathwaymediated activation of hepatic stellate cells
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摘要 肝纤维化是肝脏内弥漫性细胞外基质(特别是胶原)过度沉积的结果,如果肝纤维化进行性发展,常演变为肝硬化.而肝星状细胞的激活则是肝纤维化的核心事件,是细胞外基质分泌的主要细胞,其中的TGF-β/Smad通路是肝星状细胞内主要的信号传导通路之一,在细胞外基质的合成中起着重要作用.由于在该信号通路下游Smad复合物只能与靶基因形成松散连接,所以必然存在着相应的协同蛋白质使整个复合物紧密连接,而最近研究发现,FoxL转录因子中的FoxL2可能与整个Smad复合物形成了分子伴侣关系,他有可能加强了Smad复合物与靶基因的结合的稳定性. Hepatic fibrosis is characterized by an abnormal hepatic deposition of extracellular matrix (especially collagen).As hepatic fibrosis progresses,cirrhosis will develop.Hepatic stellate cells are the major source of the extracellular matrix(ECM).The activation of hepatic stellate cells is the central event in the development of hepatic fibrosis.The transforming growth factorbeta(TGF-β)/Smad signaling pathway plays an important role in regulating the synthesis of ECM in stellate cells.Recent studies found that forkhead L2(Fox L2),belonging to the forkhead family,was able to act as a molecular chaperone for Smad complex.Thus,it may enhance the stability between Smad complex and target genes.
作者 熊飞 李昌平
出处 《世界华人消化杂志》 CAS 北大核心 2009年第23期2396-2399,共4页 World Chinese Journal of Digestology
关键词 FOXL2 TGF-β/Smad通路 肝星状细胞 螺旋-转角-螺旋 Fox L2 TGF-β/Smad signaling pathway Hepatic stellate cell Helix-turn-helix
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