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A novel mouse model of depletion of stellate cells clarifies their role in ischemia/reperfusion- and endotoxin-induced acute liver injury

机译:星状细胞耗竭的新型小鼠模型阐明了它们在缺血/再灌注和内毒素诱导的急性肝损伤中的作用

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摘要

Background & AimsHepatic stellate cells (HSCs) that express glial fibrillary acidic protein (GFAP) are located between the sinusoidal endothelial cells and hepatocytes. HSCs are activated during liver injury and cause hepatic fibrosis by producing excessive extracellular matrix. HSCs also produce many growth factors, chemokines and cytokines, and thus may play an important role in acute liver injury. However, this function has not been clarified due to unavailability of a model in which HSCs are depleted from the normal liver.
机译:背景与目的表达神经胶质纤维酸性蛋白(GFAP)的肝星状细胞(HSC)位于正弦血管内皮细胞和肝细胞之间。 HSC在肝损伤期间被激活,并通过产生过多的细胞外基质而引起肝纤维化。造血干细胞还产生许多生长因子,趋化因子和细胞因子,因此可能在急性肝损伤中起重要作用。但是,由于无法从正常肝中清除HSCs的模型,该功能尚未阐明。

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