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PI3K/Akt/mTOR/p70S6K信号通路在肝纤维化发生发展中的作用
Association between PI3K/Akt/mTOR/p70S6K signaling pathway and hepatic fibrosis
文章发布日期:2015年10月14日  来源:  作者:吴长会,沈敏,李龙,等  点击次数:2092次  下载次数:308次

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【摘要】:PI3K/Akt/mTOR/p70S6K是细胞生命活动的重要信号通路,在促进细胞生长、增殖、侵袭、抗凋亡及促进血管生成中具有重要作用。简述了PI3K/Akt/mTOR/p70S6K信号通路作用于肝星状细胞(HSC)而对肝纤维化发生发展产生的作用,分析表明阻断该信号通路中任一靶点均能抑制HSC活化、增殖,促进HSC凋亡,抑制HSC分泌细胞外基质和延缓肝纤维化进程,阻断该通路有望成为肝纤维化的治疗策略。
【Abstract】:Phosphoinositide 3-kinase (PI3K)/protein kinase-B (AkT)/mammalian target of rapamycin (mTOR)/70-kDa ribosomal protein S6 kinase (p70S6K), PI3K/Akt/mTOR/p70S6K, is an important signaling pathway in the life activities of cells, and it plays an important role in promoting the growth, proliferation, invasion, and anti-apoptosis of cells and promoting angiogenesis. It was clarified that the PI3K/Akt/mTOR/p70S6K signaling pathway is involved in regulating the activities of hepatic stellate cell(HSC), thus influencing the development and progression of hepatic fibrosis. Analysis demonstrated that blocking any target of the PI3K/Akt/mTOR/p70S6K signaling pathway can inhibit the activation and proliferation of HSC, promote the apoptosis of HSC, inhibit the extracellular matrix secretion from HSC, and delay the progression of hepatic fibrosis. Blocking the pathway is expected to be a treatment strategy for hepatic fibrosis.
【关键字】:肝硬化;1-磷脂酰肌醇3-激酶;蛋白激酶类;哺乳动物雷帕霉素靶蛋白;核糖体蛋白质S6激酶类, 70-kDa;综述
【Key words】:liver cirrhosis; 1-phosphatidylinositol 3-kinase; protein kinases; mammalian target of rapamycin; ribosomal protein S6 kinases, 70-kDa; review
【引证本文】:吴长会, 沈敏, 李龙, 等. PI3K/Akt/mTOR/p70S6K信号通路在肝纤维化发生发展中的作用[J]. 临床肝胆病杂志, 2015, 31(11): 1928-1932.

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