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本文引用的文献

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Thyroid hormones inhibit TGF-β signaling and attenuate fibrotic responses.甲状腺激素抑制转化生长因子-β信号传导并减弱纤维化反应。
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Periostin promotes hepatic fibrosis in mice by modulating hepatic stellate cell activation via α integrin interaction.骨膜蛋白通过α整合素相互作用调节肝星状细胞活化,从而促进小鼠肝纤维化。
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Magnetic Resonance Elastography for the Evaluation of Liver Fibrosis in Chronic Hepatitis B and C by Using Both Gradient-Recalled Echo and Spin-Echo Echo Planar Imaging: A Prospective Study.利用梯度回波和自旋回波回波平面成像技术的磁共振弹性成像对慢性乙型和丙型肝炎肝纤维化的评估:一项前瞻性研究
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Signalling via the osteopontin and high mobility group box-1 axis drives the fibrogenic response to liver injury.通过骨桥蛋白和高迁移率族蛋白B1轴发出的信号驱动了对肝损伤的纤维化反应。
Gut. 2017 Jun;66(6):1123-1137. doi: 10.1136/gutjnl-2015-310752. Epub 2016 Jan 27.
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Physiological ranges of matrix rigidity modulate primary mouse hepatocyte function in part through hepatocyte nuclear factor 4 alpha.基质硬度的生理范围部分通过肝细胞核因子4α调节原代小鼠肝细胞功能。
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Normal and Fibrotic Rat Livers Demonstrate Shear Strain Softening and Compression Stiffening: A Model for Soft Tissue Mechanics.正常和纤维化大鼠肝脏表现出剪切应变软化和压缩硬化:一种软组织力学模型。
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Lysyl oxidase activity contributes to collagen stabilization during liver fibrosis progression and limits spontaneous fibrosis reversal in mice.赖氨酰氧化酶活性在肝纤维化进展过程中有助于胶原蛋白稳定,并限制小鼠自发性纤维化逆转。
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Molecular Mechanism Responsible for Fibronectin-controlled Alterations in Matrix Stiffness in Advanced Chronic Liver Fibrogenesis.晚期慢性肝纤维化中纤连蛋白控制基质硬度改变的分子机制
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指导肝纤维化中基质硬度的分子信号

Molecular Cues Guiding Matrix Stiffness in Liver Fibrosis.

作者信息

Saneyasu Takaoki, Akhtar Riaz, Sakai Takao

机构信息

MRC Centre for Drug Safety Science, Department of Molecular and Clinical Pharmacology, Institute of Translational Medicine, University of Liverpool, Liverpool L69 3GE, UK.

Centre for Materials and Structures, School of Engineering, University of Liverpool, Liverpool L69 3GE, UK.

出版信息

Biomed Res Int. 2016;2016:2646212. doi: 10.1155/2016/2646212. Epub 2016 Oct 9.

DOI:10.1155/2016/2646212
PMID:27800489
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC5075297/
Abstract

Tissue and matrix stiffness affect cell properties during morphogenesis, cell growth, differentiation, and migration and are altered in the tissue remodeling following injury and the pathological progression. However, detailed molecular mechanisms underlying alterations of stiffness are still poorly understood. Recent engineering technologies have developed powerful techniques to characterize the mechanical properties of cell and matrix at nanoscale levels. Extracellular matrix (ECM) influences mechanical tension and activation of pathogenic signaling during the development of chronic fibrotic diseases. In this short review, we will focus on the present knowledge of the mechanisms of how ECM stiffness is regulated during the development of liver fibrosis and the molecules involved in ECM stiffness as a potential therapeutic target for liver fibrosis.

摘要

组织和基质硬度在形态发生、细胞生长、分化和迁移过程中影响细胞特性,并且在损伤后的组织重塑和病理进展中发生改变。然而,硬度改变背后的详细分子机制仍知之甚少。最近的工程技术已经开发出强大的技术来表征细胞和基质在纳米尺度水平的力学性能。细胞外基质(ECM)在慢性纤维化疾病发展过程中影响机械张力和致病信号的激活。在这篇简短的综述中,我们将聚焦于目前关于肝纤维化发展过程中ECM硬度如何被调节的机制以及参与ECM硬度调节的分子的知识,这些分子可作为肝纤维化的潜在治疗靶点。