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热休克蛋白47在肝纤维化中的研究进展

Research advances on heat shock protein 47 in liver fibrosis

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【作者】 石榴韩铭袁晓雪叶峰成军蔺淑梅

【Author】 Shi Liu;Han Ming;Yuan Xiaoxue;Ye Feng;Cheng Jun;Lin Shumei;Department of Infectious Disease Medicine, the First Affiliated Hospital of Xi’an Jiaotong University;Department of Infectious Disease Research Center, Beijing Ditan Hospital,Capital Medical University;

【通讯作者】 蔺淑梅;

【机构】 西安交通大学第一附属医院感染科首都医科大学附属北京地坛医院研究所

【摘要】 肝纤维化是由胶原和非胶原在肝脏异常沉积引起,目前尚无特效治疗药物。热休克蛋白47(heat shock protein 47,HSP47)是一种存在于内质网中的胶原特异性分子伴侣,已被证实主要来源于纤维生成细胞,可协助三螺旋胶原前分子的正确折叠和稳定。在肝纤维化进程中,细胞外基质的主要来源是肝星状细胞,体内外研究均证实HSP47在肝内主要存在于肝星状细胞中,通过转化生长因子-β1(transforminggrowth factor-β1,TGF-β1)信号转导通路调控肝纤维化的发生,miRNA、HSP47-蛋白相互作用也参与了肝纤维化的发生发展,本文将对HSP47与肝纤维化的发病机制进行综述。

【Abstract】 Liver fibrosis is caused by abnormal deposition of collagen and non-collagen.However, an efficient treatment for liver fibrosis is not yet available. Heat shock protein 47(HSP47), a collagen-specific molecular chaperone residing in the endoplasmic reticulum, has been proved to assist the correct folding and stabilization of triple-helical procollagen molecules after the synthesis of polypeptide chains. In the process of liver fibrosis, studies both in vivo and in vitro have convincingly demonstrated that HSP47, which mainly found in hepatic stellate cell, regulated the occurrence of hepatic fibrosis through TGF-β1 signaling pathway. Besides,mi RNA and Hsp47-protein interaction were also involved in the development of liver fibrosis.This review retrospected the role of HSP47 on the pathogenesis and occurrence of liver fibrosis.

【基金】 国家自然科学基金面上项目(81670547);国家重点研发计划第四课题(2017YFC0908100、2017YFC0908104)
  • 【文献出处】 中国肝脏病杂志(电子版) ,Chinese Journal of Liver Diseases(Electronic Version) , 编辑部邮箱 ,2021年03期
  • 【分类号】R575.2
  • 【被引频次】1
  • 【下载频次】156
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