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| 1 | Non-invasive biomarkers for monitoring the fibrogenic process in liver:A short survey显示文摘The clinical course ofchronic liver diseases is significantly dependent on the progression rate and the extent offibrosis, i.e. the non-structured replacement of necrotic parenchyma by extracellular matrix. Fibrogenesis, i.e. the development offibrosis can be regarded as an unlimited wound healing process, which is based on matrix (connective tissue) synthesis in activated hepatic stellate cells, fibroblasts (fibrocytes), hepatocytes and biliary epithelial cells, which are converted to matrix-producing (myo-)fibroblasts by a process defined as epithelial-mesenchymal transition. Blood (noninvasive) biomarkers offibrogenesis and fibrosis can be divided into class and class analytes. Class biomarkers are those single tests, which are based on the pathophysiology offibrosis, whereas class biomarkers aremostly multiparametric algorithms, which have been statistically evaluated with regard to the detection and activity ofongoing fibrosis. Currently available markers fulfil the criteria ofideal clinical-chemical tests only partially, but increased understanding ofthe complex pathogenesis offibrosis offers additional ways for pathophysiologically well based serum (plasma) biomarkers. They include TGF-β-driven marker proteins, bone marrow-derived cells (fibrocytes), and cytokines, which govern proand anti-fibrotic activities. Proteomic and glycomic approaches ofserum are under investigation to set up specific protein or carbohydrate profiles in patients with liver fibrosis. These and other novel parameters will supplement or eventually replaceliver biopsy/histology, high resolution imaging analysis, and elastography for the detection and monitoring of patients at risk ofdeveloping liver fibrosis. | Axel M Gressner Chun-Fang Gao Olav A Gressner | 2009 | World Journal of Gastroenterology2009，15，20： | 5 |
| 2 | Connective tissue growth factor reacts as an IL-6/STAT3-regulated hepatic negative acute phase protein显示文摘AIM:To investigate the mechanisms involved in a possible modulator role of interleukin(IL) -6 signalling on CYR61-CTGF-NOV(CCN) 2/connective tissue growth factor(CTGF) expression in hepatocytes(PC) and to look for a relation between serum concentrations of these two parameters in patients with acute inflammation. METHODS:Expression of CCN2/CTGF,p-STAT3,p-Smad 3/1 and p-Smad2 was examined in primary freshly isolated rat or cryo-preserved human PC exposed to various stimuli by Western blotting,electrophoretic mobility shift assay(EMSA) ,reporter-gene-assays and reversetranscriptase polymerase chain reaction. RESULTS:IL-6 strongly down-regulated CCN2/CTGF protein and mRNA expression in PC,enhanceable by extracellular presence of the soluble IL-6 receptor gp80,and supported by an inverse relation between IL-6 and CCN2/CTGF concentrations in patients'sera.The inhi-bition of TGFβ1 driven CCN2/CTGF expression by IL-6 did not involve a modulation of Smad2(and Smad1/3) signalling.However,the STAT3 SH2 domain binding peptide,a selective inhibitor of STAT3 DNA binding activity,counteracted the inhibitory effect of IL-6 on CCN2/CTGF expression much more pronounced than pyrrolidine-dithiocarbamate,an inhibitor primarily of STAT3 phosphorylation.An EMSA confirmed STAT3 binding to the proposed proximal STAT binding site in the CCN2/CTGF promoter. CONCLUSION:CCN2/CTGF is identified as a hepatocellular negative acute phase protein which is downregulated by IL-6 via the STAT3 pathway through interaction on the DNA binding level. | Olav A Gressner Ieva Peredniene Axel M Gressner | 2011 | World Journal of Gastroenterology2011，17，2： | 3 |
| 3 | Mediators of hepatic fibrogenesis显示文摘 | Gressner A M | 1996 | Hepatogastroenterology1996，43，7： | 1 |
| 4 | Modern pathogenetic concepts of liver fibrosis suggest stellate cells and TGF-beta as major players and therapeutic targets显示文摘 | Gressner A M Weiskirchen R | 2006 | J Cell Mol Med2006，10，1： | 1 |
| 5 | Roles of TGF-beta in hepatic fibrosis显示文摘 | GRESSNER A M WEISKIRCHEN R BREITKOPF K | 2002 | Front Biosci2002，7，： | 1 |
| 6 | Modern pathogenetic concepts of liver fibrosis suggest stellate cells and TGF- beta as major players and therapeutic targets显示文摘 | Gressner A M Weiskirchen R | 2006 | J Cell Mol Med2006，10，1： | 1 |
| 7 | Roles of TGF-beta in hepatic fibrosis显示文摘 | Gressner A M Weiskirchen R Breitkopf K | 2002 | Front Biosci2002，7，： | 1 |
| 8 | Modern pathogenetic concepts of liver fibrosis suggest stellate cells and TGF-beta as major players and therapeutic targets显示文摘 | Gressner A M Weiskirchen R | 2006 | J Cell Mol Med2006，10，1： | 1 |
| 9 | Modern pathogenetic concepts of liver fibrosis suggest stellate cells and TGF-beta as major players and thera- peutic targets显示文摘 | Gressner A M Weiskirchen R | 2006 | J Cell Mol Med2006，10，1： | 1 |
| 10 | Endocrine Regulation of Energy Metabolism: Review of Pathobiochemical and Clinical Chemical Aspects of Leptin, Ghrelin, Adiponectin, and Resistin显示文摘 | Meier U Gressner A M | 2004 | Clin Chem2004，50，： | 1 |
| 11 | Modern pathogenetic concepts of liver fibrosis suggest stellate ceils and TGF hera as major players and therapeutic targets显示文摘 | Gressner A M Weiskirchen R | 2006 | J Cell Mol Med2006，10，： | 1 |
| 12 | Cytokines and cellular crosstalk involved in the activation of fat-storing cells 显示文摘 | Gressner A M | 1995 | J Hepatol1995，22，2： | 1 |
| 13 | Roles of TGF beta in hepatic fibrosis显示文摘 | GRESSNER A M | 2002 | Front Biosci2002，7，3： | 1 |
| 14 | Modern pathogenetic concepts of liver fibrosis suggest stellate cells and TGF-beta as major players and therapeutic targets显示文摘 | GRESSNER A M WEISKIRCHEN R | 2006 | J Cell Mol Med2006，10，1： | 1 |
| 15 | Roles of TGF beta in hepatic fibrosis显示文摘 | Gressner A M Weiskirchen R Breitkopf K | 2002 | Front Biosci2002，7，： | 1 |
| 16 | Expression of E-selectin ligand-1(CFR/ESL-I)on hepatic stellate cells : implications for leukocyte extravasation and liver metastasis显示文摘 | ANTOINE M TAG C G GRESSNER A M | 2009 | Oncol Rep2009，21，2： | 1 |
| 17 | Association of polymorphisms of the transforming growth factor beta1 gene with the rate of progression of HCV-induced liver fibrosis显示文摘 | Gewaltig J Mangasser-Stephan K Gartung C Biesterfeld S Gressner A M | 2002 | Clin Chim Acta2002，316，12： | 1 |
| 18 | Modem pathogenetic concepts of liver fibrosis suggest stellate cells and TGF- beta as major players and therapeutic targets 显示文摘 | Gressner A M Weiskirchen R | 2006 | J Cell Mol Med2006，10，1： | 1 |
| 19 | Modern pathogenetie concepts of liver fibrosis suggest stellate cells and TGF-beta as major players and thera- peutic targets显示文摘 | Gressner A M Weiskirchen R | 2006 | J Cell Mol Med2006，，10： | 1 |
| 20 | Modem pathogenetic concepts of liver fibrosis suggest stellate cells and TGF-beta as major players and therapeutic targets显示文摘 | GRESSNER A M WEISKIRCHEN R | 2006 | J Cell Mol Med2006，10，1： | 1 |
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