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| 1 | Gut-liver axis signaling in portal hypertension显示文摘Portal hypertension(PHT)in advanced chronic liver disease(ACLD)results from increased intrahepatic resistance caused by pathologic changes of liver tissue composition(structural component)and intrahepatic vasoconstriction(functional component).PHT is an important driver of hepatic decompensation such as development of ascites or variceal bleeding.Dysbiosis and an impaired intestinal barrier in ACLD facilitate translocation of bacteria and pathogen-associated molecular patterns(PAMPs)that promote disease progression via immune system activation with subsequent induction of proinflammatory and profibrogenic pathways.Congestive portal venous blood flow represents a critical pathophysiological mechanism linking PHT to increased intestinal permeability:The intestinal barrier function is affected by impaired microcirculation,neoangiogenesis,and abnormal vascular and mucosal permeability.The close bidirectional relationship between the gut and the liver has been termed“gut-liver axis”.Treatment strategies targeting the gut-liver axis by modulation of microbiota composition and function,intestinal barrier integrity,as well as amelioration of liver fibrosis and PHT are supposed to exert beneficial effects.The activation of the farnesoid X receptor in the liver and the gut was associated with beneficial effects in animal experiments,however,further studies regarding efficacy and safety of pharmacological FXR modulation in patients with ACLD are needed.In this review,we summarize the clinical impact of PHT on the course of liver disease,discuss the underlying pathophysiological link of PHT to gut-liver axis signaling,and provide insight into molecular mechanisms that may represent novel therapeutic targets. | Benedikt Simbrunner Mattias Mandorfer Michael Trauner Thomas Reiberger | 2019 | World Journal of Gastroenterology2019，25，39： | 6 |
| 2 | Nonselective betablocker therapy decreases intestinal permeability and serum levels of LBP and IL-6 in patients with cirrhosis显示文摘 | T. Reiberger A. Ferlitsch B.A. Payer M. Mandorfer B.B. Heinisch H. Hayden F. Lammert M. Trauner M. Peck-Radosavljevic H. Vogelsang | 2012 | Journal of Hepatology2012，，： | 5 |
| 3 | Characterization of HULC, a Novel Gene With Striking Up-Regulation in Hepatocellular Carcinoma, as Noncoding RNA显示文摘 | Katrin Panzitt Marisa M.O. Tschernatsch Christian Guelly Tarek Moustafa Martin Stradner Heimo M. Strohmaier Charles R. Buck Helmut Denk Renée Schroeder Michael Trauner Kurt Zatloukal | 2007 | Gastroenterology2007，，1： | 4 |
| 4 | Role of interleukin-1 and its antagonism of hepatic stellate cell proliferation and liver fibrosis in the Abcb4^(-/-) mouse model显示文摘AIM: To study the interleukin-1(IL-1) pathway as a therapeutic target for liver fibrosis in vitro and in vivo using the ATP-binding cassette transporter b4^(-/-)(Abcb4^(-/-)) mouse model.METHODS: Female and male Abcb4^(-/-) mice from 6 to 13 mo of age were analysed for the degree of cholestasis(liver serum tests), extent of liver fibrosis(hydroxyproline content and Sirius red staining) and tissue-specific activation of signalling pathways such as the IL-1 pathway [quantitative polymerase chain reaction(q PCR)]. For in vivo experiments, murine hepatic stellate cells(HSCs) were isolated via pronasecollagenase perfusion followed by density gradient centrifugation using female mice. Murine HSCs were stimulated with up to 1 ng/m L IL-1β with or without 2.5 μg/m L Anakinra, an IL-1 receptor antagonist, respectively. The proliferation of murine HSCs was assessed via the Brd U assay. The toxicity of Anakinra was evaluated via the fluorescein diacetate hydrolysis(FDH) assay. In vivo 8-wk-old Abcb4^(-/-) mice with an already fully established hepatic phenotype were treated with Anakinra(1 mg/kg body-weight daily intraperitoneally) or vehicle and liver injury and liver fibrosis were evaluated via serum tests, q PCR, hydroxyproline content and Sirius red staining. RESULTS: Liver fibrosis was less pronounced in males than in female Abcb4^(-/-) animals as defined by a lower hydroxyproline content(274 ± 64 μg/g vs 436 ± 80 μg/g liver, respectively; n = 13-15; P < 0.001; MannWhitney U-test) and lower m RNA expression of the profibrogenic tissue inhibitor of metalloproteinase-1(TIMP)(1 ± 0.41 vs 0.66 ± 0.33 fold, respectively; n = 13-15; P < 0.05; Mann-Whitney U-test). Reduced liver fibrosis was associated with significantly lower levels of F4/80 m RNA expression(1 ± 0.28 vs 0.71 ± 0.41 fold, respectively; n = 12-15; P < 0.05; Mann-Whitney U-test) and significantly lower IL-1β m RNA expression levels(1 ± 0.38 vs 0.44 ± 0.26 fold, respectively; n = 13-15; P < 0.001; Mann-Whitney U-test). No gender differences in the serum liver parameters [bilirubin; alanine aminotransferase(ALT); aspartate aminotransferase and alkaline phosphatase(AP)] were found. In vitro, the administration of IL-1β resulted in a significant increase in HSC proliferation [0.94 ± 0.72 arbitrary units(A.U.) in untreated controls, 1.12 ± 0.80 A.U. at an IL-1β concentration of 0.1 ng/m L and 1.18 ± 0.73 A.U. at an IL-1β concentration of 1 ng/m L in samples from n = 6 donor animals; P < 0.001; analyses of variance(ANOVA)]. Proliferation was reduced significantly by the addition of 2.5 μg/m L Anakinra(0.81 ± 0.60 A.U. in untreated controls, 0.92 ± 0.68 A.U. at an IL-1β concentration of 0.1 ng/m L, and 0.91 ± 0.69 A.U. at an IL-1β concentration of 1 ng/m L; in samples from n = 6 donor animals; P < 0.001; ANOVA) suggesting an anti-proliferative effect of this clinically approved IL-1 receptor antagonist. The FDH assay showed this dose to be non-toxic in HSCs. In vivo, Anakinra had no effect on the hepatic hydroxyprolinecontent, liver serum tests(ALT and AP) and profibrotic(collagen 1α1, collagen 1α2, transforming growth factor-β, and TIMP-1) and anti-fibrotic [matrix metalloproteinase 2(MMP2), MMP9 and MMP13 ] gene expression after 4 wk of treatment. Furthermore, the hepatic IL-1β and F4/80 m RNA expression levels were unaffected by Anakinra treatment.CONCLUSION: IL-1β expression is associated with the degree of liver fibrosis in Abcb4^(-/-) mice and promotes HSC proliferation. IL-1 antagonism shows antifibrotic effects in vitro but not in Abcb4^(-/-) mice. | Florian P Reiter Ralf Wimmer Lena Wottke Renate Artmann Jutta M Nagel Manuel O Carranza Doris Mayr Christian Rust Peter Fickert Michael Trauner Alexander L Gerbes Simon Hohenester Gerald U Denk | 2016 | World Journal of Hepatology2016，8，8： | 3 |
| 5 | Endoscopic radiofrequency ablation for malignant biliary obstruction: a nationwide retrospective study of 84 consecutive applications显示文摘 | Werner Dolak Florian Schreiber Hubert Schwaighofer Michael Gschwantler Wolfgang Plieschnegger Alexander Ziachehabi Andreas Mayer Ludwig Kramer Andreas Kopecky Christiane Schrutka-K?lbl Gernot Wolkersd?rfer Christian Madl Frieder Berr Michael Trauner Andre | 2014 | Surgical Endoscopy2014，，3： | 3 |
| 6 | Hepatotoxicity of NONI juice: Report of two cases显示文摘NONI juice (Morinda citrifolia) is an increasingly popular wellness drink claimed to be beneficial for many illnesses.No overt toxicity has been reported to date. We present two cases of novel hepatotoxicity of NONI juice. Causality of liver injury by NONI juice was asses-sed. Routine laboratory tests and transjugular or percutaneous liver biopsy were performed. The first patient underwent successful liver transplantation while the second patient recovered spontaneously after cessation of NONI juice.A 29-year-old man with previous toxic hepatitis associated with small doses of paracetamol developed sub-acute hepatic failure following consumption of 1.5 L NONI juice over 3 wk necessitating urgent liver transplantation. A 62-year-old woman without evidence of previous liver disease developed an episode of self-limited acutehepatitis following consumption of 2 L NONI juice for over 3 mo. The most likely hepatotoxic components of Morinda citrifolia were anthraquinones. Physicians should be aware of potential hepatotoxicity of NONI juice. | Vanessa Stadlbauer Peter Fickert Carolin Lackner Jutta Schmerlaib Peter Krisper Michael Trauner Rudolf E Stauber | 2005 | World Journal of Gastroenterology2005，11，30： | 3 |
| 7 | Non-selective β Blockers Increase Risk for Hepatorenal Syndrome and Death in Patients with Cirrhosis and Spontaneous Bacterial Peritonitis显示文摘 | Mattias Mandorfer Simona Bota Philipp Schwabl Theresa Bucsics Nikolaus Pfisterer Matthias Kruzik Michael Hagmann Alexander Blacky Arnulf Ferlitsch Wolfgang Sieghart Michael Trauner Markus Peck-Radosavljevic Thomas Reiberger | 2014 | Gastroenterology2014，，： | 3 |
| 8 | Selective Activation of Nuclear Bile Acid Receptor FXR in the Intestine Protects Mice Against Cholestasis显示文摘 | Salvatore Modica Michele Petruzzelli Elena Bellafante Stefania Murzilli Lorena Salvatore Nicola Celli Giuseppe Di Tullio Giuseppe Palasciano Tarek Moustafa Emina Halilbasic Michael Trauner Antonio Moschetta | 2012 | Gastroenterology2012，，2： | 2 |
| 9 | Carvedilol for primary prophylaxis of variceal bleeding in cirrhotic patients with haemodynamic non-response to propranolol显示文摘 | Thomas Reiberger Gregor Ulbrich Arnulf Ferlitsch Berit Anna Payer Philipp Schwabl Matthias Pinter Birgit B Heinisch Michael Trauner Ludwig Kramer Markus Peck-Radosavljevic | 2013 | Gut2013，，11： | 2 |
| 10 | Multicenter analysis of soluble A xl reveals diagnostic value for very early stage hepatocellular carcinoma显示文摘 | Patrick Reichl Meng Fang Patrick Starlinger Katharina Staufer Rudolf Nenutil Petr Muller Kristina Greplova Dalibor Valik Steven Dooley Christine Brostjan Thomas Gruenberger Jiayun Shen Kwan Man Michael Trauner Jun Yu Chun Fang Gao Wolfgang Mikulits | 2015 | Int. J. Cancer2015，，2： | 2 |
| 11 | How to STATE suitability and START transarterial chemoembolization in patients with intermediate stage hepatocellular carcinoma显示文摘 | Florian Hucke Matthias Pinter Ivo Graziadei Simona Bota Wolfgang Vogel Christian Müller Harald Heinzl Fredrik Waneck Michael Trauner Markus Peck-Radosavljevic Wolfgang Sieghart | 2014 | Journal of Hepatology2014，，： | 2 |
| 12 | A randomized head-to-head study of small-bowel imaging comparing MiroCam and EndoCapsule显示文摘 | W. Dolak S. Kulnigg-Dabsch R. Evstatiev C. Gasche M. Trauner A. Püsp?k | 2012 | Endoscopy2012，，11： | 2 |
| 13 | Von Willebrand factor as new noninvasive predictor of portal hypertension, decompensation and mortality in patients with liver cirrhosis显示文摘 | Monika Ferlitsch Thomas Reiberger Matthias Hoke Petra Salzl Bernadette Schwengerer Gregor Ulbrich Berit Anna Payer Michael Trauner Markus Peck‐Radosavljevic Arnulf Ferlitsch | 2012 | Hepatology2012，，4： | 2 |
| 14 | Prevalence of flat lesions in a large screening population and their role in colonoscopy quality improvement显示文摘 | K. Reinhart C. Bannert D. Dunkler P. Salzl M. Trauner F. Renner P. Knoflach A. Ferlitsch W. Weiss M. Ferlitsch | 2013 | Endoscopy2013，，05： | 2 |
| 15 | Pathogenesis of primary sclerosing cholangitis显示文摘 | Marion J. Pollheimer Emina Halilbasic Peter Fickert Michael Trauner | 2011 | Best Practice & Research Clinical Gastroenterology2011，，6： | 1 |
| 16 | New paradigms in the treatment of hepatic cholestasis:from UDCA to FXR,PXR and beyond显示文摘 | Beuers U Trauner M Jansen P | 2015 | J Hepatol2015，，： | 1 |
| 17 | Nuclear receptors as therapeutic targets in cholestatic liver diseases显示文摘 | Zollner G Trauner M | 2009 | Br J Pharmacol2009，156，1： | 1 |
| 18 | Expression of the bile salt export pump is maintained after chronic cholestasis in the rat 显示文摘 | Lee JM Trauner M Soroka CJ | 2000 | Gastroenterology2000，118，1： | 1 |
| 19 | MDR3(ABCB4)defects:a paradigm for the gentics of adult cholestatic syndromes显示文摘 | Trauner M Ficker P Wsgner M | | 0，，： | 1 |
| 20 | New paradigms in the treatment of hepatic cholestasis:from UDCA to FXR,PXR and beyond显示文摘 | Beuers U Trauner M Jansen P et a1 | 2015 | J Hepatol2015，，： | 1 |
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