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Progress of Targeting Transforming Growth Factor-β1 Small Interfering RNA in Liver Fibrosis

机译:肝纤维化靶向转化生长因子β1小干扰RNA的研究进展

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摘要

Liver fibrosis is a common pathological consequence of a variety of chronic stimuli, including viral, autoimmune, drug-induced, cholestatic and metabolic diseases. Fibrosis is driven by a dynamic process involving increased synthesis of matrix components and a failure of physiological mechanisms of matrix turnover. Activation of hepatic stellate cells (HSCs) remains a central event in fibrosis. HSCs are the main source of extracellular matrix (ECM). Transforming growth factor-beta (TGF-β), which is the fibrogenic master cytokine, can induce the activation of HSCs to produce a large amount of ECM, and is capable of inducing apoptosis of liver cells. RNA interference (RNAi) is a novel gene disruption technology. Studies have shown that small interfering RNA (siRNA) targeting TGF-β1 may inhibit the activation and proliferation of HSCs, suppress ECM synthesis and block liver fibrosis. TGF-β1 siRNA-mediated gene silencing therapy provides a new avenue for liver fibrosis. This review summarizes recent progresses in research on HSCs, TGF-β1 and TGF-β1 siRNA in liver fibrosis.
机译:肝纤维化是多种慢性刺激的常见病理结果,包括病毒性,自身免疫性,药物诱导性,胆汁淤积性和代谢性疾病。纤维化是由一个动态过程驱动的,该过程涉及基质成分合成的增加以及基质周转的生理机制的失败。肝星状细胞(HSC)的激活仍然是纤维化的中心事件。造血干细胞是细胞外基质(ECM)的主要来源。转化生长因子-β(TGF-β)是纤维化的主细胞因子,可诱导HSC活化,从而产生大量ECM,并能够诱导肝细胞凋亡。 RNA干扰(RNAi)是一种新颖的基因破坏技术。研究表明,靶向TGF-β1的小干扰RNA(siRNA)可能抑制HSC的激活和增殖,抑制ECM合成并阻止肝纤维化。 TGF-β1siRNA介导的基因沉默疗法为肝纤维化提供了新途径。综述了肝纤维化中HSC,TGF-β1和TGF-β1siRNA的最新研究进展。

著录项

  • 来源
    《中国医学科学杂志(英文版)》 |2014年第4期|231-235|共5页
  • 作者

    Xuan Zhou; Xue-feng Yang;

  • 作者单位

    Department of Gastroenterology, Affiliated Nanhua Hospital, University of South China, Hengyang, Hunan 421002, China;

    Department of Gastroenterology, Affiliated Nanhua Hospital, University of South China, Hengyang, Hunan 421002, China;

  • 收录信息 中国科学引文数据库(CSCD);中国科技论文与引文数据库(CSTPCD);
  • 原文格式 PDF
  • 正文语种 eng
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