Liver fibrosis

被引：467

作者：

Aydin, M. Merve ^{[1
]}

Akcali, Kamil Can ^{[2
]}

机构：

[1] Mikrogen Genet Diagnost Lab, Ankara, Turkey

[2] Ankara Univ, Sch Med, Dept Biophys, Ankara, Turkey

来源：

TURKISH JOURNAL OF GASTROENTEROLOGY | 2018年 / 29卷 / 01期

关键词：

Fibrosis; liver; MMPs; experimental models; HEPATIC STELLATE CELLS; CHOLINE-DEFICIENT; NONALCOHOLIC STEATOHEPATITIS; PROTEOMIC ANALYSIS; OXIDATIVE STRESS; ANIMAL-MODELS; NADPH OXIDASE; RECEPTOR; B-VIRUS; MICE;

D O I：

10.5152/tjg.2018.17330

中图分类号：

R57 [消化系及腹部疾病];

学科分类号：

100201 [内科学];

摘要：

Liver fibrosis is a wound-healing response generated against an insult to the liver that causes liver injury. It has the potential to progress into cirrhosis, and if not prevented, it may lead to liver cancer and liver failure. The activation of hepatic stellate cells (HSCs) is the central event underlying liver fibrosis. In addition to HSCs, numerous studies have supported the potential contribution of bone marrow-derived cells and myofibroblasts to liver fibrosis. The liver is a heterogeneous organ; thus, molecular and cellular events that underlie liver fibrogenesis are complex. This review aims to focus on major events that occur during liver fibrogenesis. In addition, important antifibrotic therapeutic approaches and experimental liver fibrosis models will be discussed.

引用

收藏

页码：14 / 21

页数：8

相关论文

共 89 条

[1]

Mouse models in non-alcoholic fatty liver disease and steatohepatitis research [J].

Anstee, QM ;

Goldin, RD .

INTERNATIONAL JOURNAL OF EXPERIMENTAL PATHOLOGY, 2006, 87 (01) :1-16

[2]

Comparative proteomic analysis of thiol proteins in the liver after oxidative stress induced by diethylnitrosamine [J].

Aparicio-Bautista, Diana I. ;

Perez-Carreon, Julio I. ;

Gutierrez-Najera, Nora ;

Reyes-Grajeda, Juan P. ;

Arellanes-Robledo, Jaime ;

Vasquez-Garzon, Veronica R. ;

Jimenez-Garcia, Monica N. ;

Villa-Trevino, Saul .

BIOCHIMICA ET BIOPHYSICA ACTA-PROTEINS AND PROTEOMICS, 2013, 1834 (12) :2528-2538

[3]

Reversibility and heritability of liver fibrosis: Implications for research and therapy [J].

Atta, Hussein M. .

WORLD JOURNAL OF GASTROENTEROLOGY, 2015, 21 (17) :5138-5148

[4]

Pharmacological inhibition of the chemokine CCL2 (MCP-1) diminishes liver macrophage infiltration and steatohepatitis in chronic hepatic injury [J].

Baeck, Christer ;

Wehr, Alexander ;

Karlmark, Karlin Raja ;

Heymann, Felix ;

Vucur, Mihael ;

Gassler, Nikolaus ;

Huss, Sebastian ;

Klussmann, Sven ;

Eulberg, Dirk ;

Luedde, Tom ;

Trautwein, Christian ;

Tacke, Frank .

GUT, 2012, 61 (03) :416-426

[5]

Clinical Advancements in the Targeted Therapies against Liver Fibrosis [J].

Bansal, Ruchi ;

Nagorniewicz, Beata ;

Prakash, Jai .

MEDIATORS OF INFLAMMATION, 2016, 2016

[6]

Liver fibrosis [J].

Bataller, R ;

Brenner, DA .

JOURNAL OF CLINICAL INVESTIGATION, 2005, 115 (02) :209-218

[7]

Mechanisms and cell signaling in alcoholic liver disease [J].

Beier, Juliane I. ;

McClain, Craig J. .

BIOLOGICAL CHEMISTRY, 2010, 391 (11) :1249-1264

[8]

TGF-β/Smad signaling in the injured liver [J].

Breitkopf, K ;

Godoy, P ;

Ciuclan, L ;

Singer, MV ;

Dooley, S .

ZEITSCHRIFT FUR GASTROENTEROLOGIE, 2006, 44 (01) :57-66

[9]

The basement membrane component of biologic scaffolds derived from extracellular matrix [J].

Brown, B ;

Lindberg, K ;

Reing, J ;

Stolz, DB ;

Badylak, SF .

TISSUE ENGINEERING, 2006, 12 (03) :519-526

[10]

Molecular mechanisms and clinical applications of angiogenesis [J].

Carmeliet, Peter ;

Jain, Rakesh K. .

NATURE, 2011, 473 (7347) :298-307

← 1 2 3 4 5 6 7 8 9 →