Christian Trautwein

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About Christian Trautwein:

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SEEK ID: https://seek.lisym.org/people/104

Location: Germany

ORCID: Not specified

Joined: 27th Apr 2018

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LiSyM-Krebs - Systemmedizinisches Forschungsnetz zur Früherkennung und Prävention von Leberkrebs

LiSyM-Krebs ist ein nationales Forschungsnetz zur Früherkennung und Prävention von Leberkrebs, das unter Verwendung des systemmedizinischen Forschungsansatzes die komplexen, dynamischen Prozesse der Krankheitsprogression analysiert, um ausgehend von den Erkenntnissen aus dem Forschungsnetz LiSyM die Entstehung von Leberkrebs besser zu verstehen, vorherzusagen und im besten Fall sogar zu verhindern. LiSyM-Krebs setzt die erfolgreichen Forschungsaktivitäten der BMBF-Vorgängerprogramme ...

Projects: LiSyM-Krebs Partnering, Forschungsnetzwerk LiSyM-Krebs, SMART-NAFLD, DEEP-HCC network, C-TIP-HCC network

Web page: https://www.lisym-cancer.org

LiSyM: Liver Systems Medicine

Liver Systems Medicine : striving to develop non-invasive methods for diagnosing and treating NAFLD by combining mathematical modeling and biological research. LiSyM, is a multidisciplinary research network, in which molecular and cell biologists, clinical researchers, pharmacologists and experts in mathematical modeling examine the liver in its entirety. LiSyM research focuses on the metabolic liver disease non-alcoholic fatty liver disease (NAFLD), which includes non-alcoholic steatohepatitis ...

Projects: LiSyM Core Infrastructure and Management (LiSyM-PD), LiSyM Pillar I: Early Metabolic Injury (LiSyM-EMI), LiSyM Pillar II: Chronic Liver Disease Progression (LiSyM-DP), LiSyM Pillar III: Regeneration and Repair in Acute-on-Chronic Liver Failure (LiSyM-ACLF), LiSyM Pillar IV: Liver Function Diagnostics (LiSyM-LiFuDi), Model Guided Pharmacotherapy In Chronic Liver Disease (LiSyM-MGP), Molecular Steatosis - Imaging & Modeling (LiSyM-MSIM), The Hedgehog Signalling Pathway (LiSyM-JGMMS), Multi-Scale Models for Personalized Liver Function Tests (LiSyM-MM-PLF), LiSyM PALs, Project Management PTJ, LiSyM network, LiSyM Scientific Leadership Team (LiSyM-LT)

Web page: https://www.lisym.org/

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LiSyM-Krebs Partnering

This generic project is intended to be a forum for all LiSyM partner and external stakeholders interested in participating in the BMBF initiative LiSyM-Krebs.

Programme: LiSyM-Krebs - Systemmedizinisches Forschungsnetz zur Früherkennung und Prävention von Leberkrebs

Public web page: https://www.ptj.de/projektfoerderung/gesundheitsforschung/lisym-krebs

Organisms: Not specified

LiSyM network

This comprises the whole LiSyM network

Programme: LiSyM: Liver Systems Medicine

Public web page: http://www.lisym.org

Start date: 1st Jan 2016

Organisms: Rattus norvegicus, Rattus rattus, Mus musculus, Homo sapiens

LiSyM Pillar II: Chronic Liver Disease Progression (LiSyM-DP)

In one in five people with NAFLD, the functioning liver cells, the hepatocytes, are replaced by connective tissue. Eventually this fibrosis becomes irreversible. In this state the liver is like a ‘scar that never heals’. Through it, the liver loses many of its vital functions. LiSyM-Pillar II wants to know more about which factors promote fibrosis and the conditions under which fibrosis becomes irreversible How can fibrosis be diagnosed as early as possible? Researchers in the pillar are also ...

Programme: LiSyM: Liver Systems Medicine

Public web page: http://www.lisym.org/our-work/pillar-research

Start date: 1st Jan 2016

Organisms: Mus musculus, Rattus rattus, Rattus norvegicus, Homo sapiens

LiSyM Scientific Leadership Team (LiSyM-LT)

Day-to-day science within the LiSyM is overseen and directed by the the LiSyM Scientific Leadership Team. This coordination team comprises the pillar coordinators and additional LiSyM members, and ensures smooth interaction between multi-skilled groups, often working in different institutions and across significant distances within Germany.

Programme: LiSyM: Liver Systems Medicine

Public web page: http://www.lisym.org/who-we-are

Organisms: Not specified

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RWTH Aachen University Hospital - Department of Internal Medicine III

Country: Germany

City: 52074 Aachen

Web page: https://www.ukaachen.de/kliniken-institute/klinik-fuer-gastroenterologie-stoffwechselerkrankungen-und-internistische-intensivmedizin-med-klinik-iii.html

Showing 10 out of a possible 11 Publications Advanced Publications list for this Person with search and filtering

Transcriptomic Cross‐Species Analysis of Chronic Liver Disease Reveals Consistent Regulation Between Humans and Mice

LiSyM Pillar II: Chronic Liver Disease Progression (LiSyM-DP)

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Abstract

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Authors: Christian H. Holland, Ricardo O. Ramirez Flores, Maiju Myllys, Reham Hassan, Karolina Edlund, Ute Hofmann, Rosemarie Marchan, Cristina Cadenas, Jörg Reinders, Stefan Hoehme, Abdel‐latif Seddek, Steven Dooley, Verena Keitel, Patricio Godoy, Brigitte Begher‐Tibbe, Christian Trautwein, Christian Rupp, Sebastian Mueller, Thomas Longerich, Jan G. Hengstler, Julio Saez‐Rodriguez, Ahmed Ghallab

Date Published: 28th Aug 2021

Publication Type: Journal

DOI: 10.1002/hep4.1797

Citation: Hepatol Commun,hep4.1797

Created: 28th Aug 2021 at 09:39, Last updated: 8th Mar 2024 at 07:44

Unexpected Pro-Fibrotic Effect of MIF in Non-Alcoholic Steatohepatitis Is Linked to a Shift in NKT Cell Populations

LiSyM Pillar II: Chronic Liver Disease Progression (LiSyM-DP)

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Macrophage migration inhibitory factor (MIF) is a pleiotropic inflammatory cytokine with anti-fibrotic properties in toxic liver injury models and anti-steatotic functions in non-alcoholic fatty liver …

Authors: D. Heinrichs, E. F. Brandt, P. Fischer, Janine Koehncke, Theresa H. Wirtz, N. Guldiken, S. Djudjaj, P. Boor, D.Kroy, R. Weiskirchen, Richard Bucala, H.E. Wasmuth, P. Strnad, Christian Trautwein, J. Bernhagen, M. L. Berres

Date Published: 28th Jan 2021

Publication Type: Journal

DOI: 10.3390/cells10020252

Citation:

Created: 28th Jan 2021 at 11:32, Last updated: 8th Mar 2024 at 07:44

Hepatocyte-specific NRF2 activation controls fibrogenesis and carcinogenesis in steatohepatitis.

LiSyM Pillar IV: Liver Function Diagnostics (LiSyM-LiFuDi)

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BACKGROUND & AIMS: In chronic liver diseases, inflammation induces oxidative stress and thus may contribute to the progression of liver injury, fibrosis, and carcinogenesis. The KEAP1/NRF2 axis is … a major regulator of cellular redox balance. In the present study, we investigated whether the KEAP1/NRF2 system is involved in liver disease progression in humans and mice. METHODS: The clinical relevance of oxidative stress was investigated by liver RNA sequencing in a well-characterized cohort of patients with non-alcoholic fatty liver disease (n = 63) and correlated with histological and clinical parameters. For functional analysis, hepatocyte-specific Nemo knockout (NEMO(Deltahepa)) mice were crossed with hepatocyte-specific Keap1 knockout (KEAP1(Deltahepa)) mice. RESULTS: Immunohistochemical analysis of human liver sections showed increased oxidative stress and high NRF2 expression in patients with chronic liver disease. RNA sequencing of liver samples in a human pediatric NAFLD cohort revealed a significant increase of NRF2 activation correlating with the grade of inflammation, but not with the grade of steatosis, which could be confirmed in a second adult NASH cohort. In mice, microarray analysis revealed that Keap1 deletion induces NRF2 target genes involved in glutathione metabolism and xenobiotic stress (e.g., Nqo1). Furthermore, deficiency of one of the most important antioxidants, glutathione (GSH), in NEMO(Deltahepa) livers was rescued after deleting Keap1. As a consequence, NEMO(Deltahepa)/KEAP1(Deltahepa) livers showed reduced apoptosis compared to NEMO(Deltahepa) livers as well as a dramatic downregulation of genes involved in cell cycle regulation and DNA replication. Consequently, NEMO(Deltahepa)/KEAP1(Deltahepa) compared to NEMO(Deltahepa) livers displayed decreased fibrogenesis, lower tumor incidence, reduced tumor number, and decreased tumor size. CONCLUSIONS: NRF2 activation in patients with non-alcoholic steatohepatitis correlates with the grade of inflammation, but not steatosis. Functional analysis in mice demonstrated that NRF2 activation in chronic liver disease is protective by ameliorating fibrogenesis, initiation and progression of hepatocellular carcinogenesis. LAY SUMMARY: The KEAP1 (Kelch-like ECH-associated protein-1)/NRF2 (erythroid 2-related factor 2) axis has a major role in regulating cellular redox balance. Herein, we show that NRF2 activity correlates with the grade of inflammation in patients with non-alcoholic steatohepatitis. Functional studies in mice actually show that NRF2 activation, resulting from KEAP1 deletion, protects against fibrosis and cancer.

Authors: A. Mohs, T. Otto, K. M. Schneider, M. Peltzer, M. Boekschoten, C. H. Holland, C. A. Hudert, L. Kalveram, S. Wiegand, J. Saez-Rodriguez, T. Longerich, J. G. Hengstler, C. Trautwein

Date Published: 22nd Dec 2020

Publication Type: Journal

PubMed ID: 33342543

Citation: J Hepatol. 2021 Mar;74(3):638-648. doi: 10.1016/j.jhep.2020.09.037. Epub 2020 Oct 24.

Created: 29th Jun 2021 at 17:25, Last updated: 8th Mar 2024 at 07:44

Balance between macrophage migration inhibitory factor and sCD74 predicts outcome in patients with acute decompensation of cirrhosis

LiSyM Pillar II: Chronic Liver Disease Progression (LiSyM-DP)

Abstract

Not specified

Authors: Theresa H. Wirtz, Philipp A. Reuken, Christian Jansen, Petra Fischer, Irina Bergmann, Christina Backhaus, Christoph Emontzpohl, Johanna Reißing, Elisa F. Brandt, M. Teresa Koenen, Kai M. Schneider, Robert Schierwagen, Maximilian J. Brol, Johannes Chang, Henning W. Zimmermann, Nilay Köse-Vogel, Thomas Eggermann, Ingo Kurth, Christian Stoppe, Richard Bucala, Jürgen Bernhagen, Michael Praktiknjo, Andreas Stallmach, Christian Trautwein, Jonel Trebicka, Tony Bruns, Marie-Luise Berres

Date Published: 1st Dec 2020

Publication Type: Journal

DOI: 10.1016/j.jhepr.2020.100221

Citation: JHEP Reports:100221

Created: 28th Jan 2021 at 11:18, Last updated: 8th Mar 2024 at 07:44

Hepatocyte-specific NRF2 activation controls fibrogenesis and carcinogenesis in steatohepatitis

LiSyM Pillar II: Chronic Liver Disease Progression (LiSyM-DP)

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Background & Aims Inflammation in chronic liver diseases induces oxidative stress and thus may contribute to progression of liver injury, fibrosis, and carcinogenesis. The KEAP1/NRF2 axis is a major …

Authors: Antje Mohs, Tobias Otto, Kai Markus Schneider, Mona Peltzer, Mark Boekschoten, Christian H. Holland, Christian A. Hudert, Laura Kalveram, Susanna Wiegand, Julio Saez-Rodriguez, Thomas Longerich, Jan G. Hengstler, Christian Trautwein

Date Published: 1st Oct 2020

Publication Type: Journal

DOI: 10.1016/j.jhep.2020.09.037

Citation: Journal of Hepatology,S0168827820336953

Created: 27th Oct 2020 at 10:09, Last updated: 8th Mar 2024 at 07:44

Lipid-encapsulated siRNA for hepatocyte-directed treatment of advanced liver disease

LiSyM Pillar II: Chronic Liver Disease Progression (LiSyM-DP), LiSyM Pillar III: Regeneration and Repair in Acute-on-Chronic Liver Failure (LiSyM-ACLF), LiSyM network

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Lipid-based RNA nanocarriers have been recently accepted as a novel therapeutic option in humans, thus increasing the therapeutic options for patients. Tailored nanomedicines will enable to treat chronic …

Authors: Marius Maximilian Woitok, Miguel Eugenio Zoubek, Dennis Doleschel, Matthias Bartneck, Mohamed Ramadan Mohamed, Fabian Kießling, Wiltrud Lederle, Christian Trautwein, Francisco Javier Cubero

Date Published: 1st May 2020

Publication Type: Journal

DOI: 10.1038/s41419-020-2571-4

Citation: Cell Death Dis 11(5),343

Created: 26th Jul 2020 at 18:48, Last updated: 8th Mar 2024 at 07:44

Influence of Liver Fibrosis on Lobular Zonation

Model Guided Pharmacotherapy In Chronic Liver Disease (LiSyM-MGP)

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Little is known about how liver fibrosis influences lobular zonation. To address this question, we used three mouse models of liver fibrosis, repeated CCl4 administration for 2, 6 and 12 months to …

Authors: Ahmed Ghallab, Maiju Myllys, Christian Holland, Ayham Zaza, Walaa Murad, Reham Hassan, Yasser A Ahmed, Tahany Abbas, Eman Abdelrahim, Kai Markus Schneider, Madlen Matz-Soja, Joerg Reinders, Rolf Gebhardt, Theresa Hildegard Wirtz, Maximilian Hatting, Dirk Drasdo, Julio Saez-Rodriguez, Christian Trautwein, Jan Hengstler

Date Published: 1st Dec 2019

Publication Type: Not specified

DOI: 10.3390/cells8121556

Citation: Cells 8(12):1556 2019

Created: 5th Dec 2019 at 08:42, Last updated: 8th Mar 2024 at 07:44

Genetic Variants in the Promoter Region of the Macrophage Migration Inhibitory Factor are Associated with the Severity of Hepatitis C Virus-Induced Liver Fibrosis.

LiSyM Pillar II: Chronic Liver Disease Progression (LiSyM-DP)

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Two polymorphisms in the promoter region of macrophage migration inhibitory factor (MIF) - rs755622 and rs5844572 - exhibit prognostic relevance in inflammatory diseases. The aim of this study was to …

Authors: T. H. Wirtz, P. Fischer, C. Backhaus, I. Bergmann, E. F. Brandt, D. Heinrichs, M. T. Koenen, K. M. Schneider, T. Eggermann, I. Kurth, C. Stoppe, J. Bernhagen, T. Bruns, J. Fischer, T. Berg, C. Trautwein, M. L. Berres

Date Published: 31st Jul 2019

Publication Type: Journal

PubMed ID: 31370326

Citation: Int J Mol Sci. 2019 Jul 31;20(15). pii: ijms20153753. doi: 10.3390/ijms20153753.

Created: 27th Jul 2020 at 12:54, Last updated: 8th Mar 2024 at 07:44

Liver Fibrosis and Metabolic Alterations in Adults With alpha-1-antitrypsin Deficiency Caused by the Pi*ZZ Mutation.

LiSyM Pillar III: Regeneration and Repair in Acute-on-Chronic Liver Failure (LiSyM-ACLF), LiSyM network

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BACKGROUND & AIMS: Alpha-1 antitrypsin deficiency (AATD) is among the most common genetic disorders. Severe AATD is caused by a homozygous mutation in the SERPINA1 gene that encodes the Glu342Lys … substitution (called the Pi*Z mutation, Pi*ZZ genotype). Pi*ZZ carriers may develop lung and liver diseases. Mutation-associated lung disorders have been well studied, but less is known about the effects in liver. We assessed the liver disease burden and associated features in adults with this form of AATD. METHODS: We collected data from 554 Pi*ZZ adults (403 in an exploratory cohort, 151 in a confirmatory cohort), in 9 European countries, with AATD who were homozygous for the Pi*Z mutation, and 234 adults without the Pi*Z mutation (controls), all without pre-existing liver disease. We collected data on demographic parameters, comorbidities, lung- and liver-related health, and blood samples for laboratory analysis. Liver fibrosis was assessed non-invasively via the serum tests Aspartate Aminotransferase to Platelet Ratio Index and HepaScore and via transient elastography. Liver steatosis was determined via transient elastography-based controlled attenuation parameter. We performed histologic analyses of livers from transgenic mice that overexpress the AATD-associated Pi*Z variant. RESULTS: Serum levels of liver enzymes were significantly higher in Pi*ZZ carriers vs controls. Based on non-invasive tests for liver fibrosis, significant fibrosis was suspected in 20%-36% of Pi*ZZ carriers, whereas signs of advanced fibrosis were 9- to 20-fold more common in Pi*ZZ carriers compared to non-carriers. Male sex; age older than 50 years; increased levels of alanine aminotransferase, aspartate aminotransferase, or gamma-glutamyl transferase; and low numbers of platelets were associated with higher liver fibrosis burden. We did not find evidence for a relationship between lung function and liver fibrosis. Controlled attenuation parameter >/=280 dB/m, suggesting severe steatosis, was detected in 39% of Pi*ZZ carriers vs 31% of controls. Carriers of Pi*ZZ had lower serum concentrations of triglyceride and low- and very-low-density lipoprotein cholesterol than controls, suggesting impaired hepatic secretion of lipid. Livers from Pi*Z-overexpressing mice had steatosis and down-regulation of genes involved in lipid secretion. CONCLUSIONS: In studies of AATD adults with the Pi*ZZ mutation, and of Pi*Z-overexpressing mice, we found evidence of liver steatosis and impaired lipid secretion. We identified factors associated with significant liver fibrosis in patients, which could facilitate hepatologic assessment and counseling of individuals who carry the Pi*ZZ mutation. ClinicalTrials.gov Number NCT02929940.

Authors: K. Hamesch, M. Mandorfer, V. M. Pereira, L. S. Moeller, M. Pons, G. E. Dolman, M. C. Reichert, C. V. Schneider, V. Woditsch, J. Voss, C. Lindhauer, M. Fromme, I. Spivak, N. Guldiken, B. Zhou, A. Arslanow, B. Schaefer, H. Zoller, E. Aigner, T. Reiberger, M. Wetzel, B. Siegmund, C. Simoes, R. Gaspar, L. Maia, D. Costa, M. Bento-Miranda, J. van Helden, E. Yagmur, D. Bzdok, J. Stolk, W. Gleiber, V. Knipel, W. Windisch, R. Mahadeva, R. Bals, R. Koczulla, M. Barrecheguren, M. Miravitlles, S. Janciauskiene, F. Stickel, F. Lammert, R. Liberal, J. Genesca, W. J. Griffiths, M. Trauner, A. Krag, C. Trautwein, P. Strnad