Matthias Reichert

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About Matthias Reichert:

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SEEK ID: https://seek.lisym.org/people/19

Location: Germany

ORCID: Not specified

Joined: 28th Apr 2017

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

In chronic diseases, at some point the liver can suddenly stop functioning. This is called acute-on-chronic liver failure, or ACLF. This is the leading cause of death in liver patients and is often provoked by the use of transcription or freely available drugs or alcohol abuse. For this condition we need an effective treatment quickly. LiSyM-Pillar III researches the factors that contribute significantly to ACLF. What exactly happens then? Are there any early signs that would enable ACLF to be ...

Programme: LiSyM: Liver Systems Medicine

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

Start date: 1st Jan 2016

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

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 PALs

This is a generic project that comprises all LiSyM data management PALs and associated FAIRDOM PALs, as well as the LiSyM data management team. Olga Maja Alain

Programme: LiSyM: Liver Systems Medicine

Public web page: Not specified

Organisms: Not specified

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Saarland University Hospital - Department of Medicine II

Country: Germany

City: 66421 Homburg/Saar

Web page: http://www.uniklinikum-saarland.de/einrichtungen/kliniken_institute/medizinische_kliniken/innere_medizin_ii

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

Isolated bacterial infection without decompensation has no impact on survival of compensated patients with cirrhosis.

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

Abstract (Expand)

BACKGROUND & AIMS: Bacterial infections (BI) affect the natural course of cirrhosis and were suggested to be a landmark event marking the transition to the decompensated stage. Our specific aim was …

Authors: M. C. Reichert, C. Schneider, R. Greinert, M. Casper, F. Grunhage, A. Wienke, A. Zipprich, F. Lammert, C. Ripoll

Date Published: 1st Mar 2021

Publication Type: Journal

PubMed ID: 33641234

Citation: Liver Int. 2021 Jun;41(6):1370-1378. doi: 10.1111/liv.14842. Epub 2021 Mar 14.

Created: 30th Jun 2021 at 08:17, Last updated: 8th Mar 2024 at 07:44

rs641738C>T near MBOAT7 is associated with liver fat, ALT and fibrosis in NAFLD: A meta-analysis.

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

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BACKGROUND & AIMS: A common genetic variant near MBOAT7 (rs641738C>T) has been previously associated with hepatic fat and advanced histology in NAFLD; however, these findings have not been … consistently replicated in the literature. We aimed to establish whether rs641738C>T is a risk factor across the spectrum of NAFLD and to characterise its role in the regulation of related metabolic phenotypes through a meta-analysis. METHODS: We performed a meta-analysis of studies with data on the association between rs641738C>T genotype and liver fat, NAFLD histology, and serum alanine aminotransferase (ALT), lipids or insulin. These included directly genotyped studies and population-level data from genome-wide association studies (GWAS). We performed a random effects meta-analysis using recessive, additive and dominant genetic models. RESULTS: Data from 1,066,175 participants (9,688 with liver biopsies) across 42 studies were included in the meta-analysis. rs641738C>T was associated with higher liver fat on CT/MRI (+0.03 standard deviations [95% CI 0.02-0.05], pz = 4.8x10(-5)) and diagnosis of NAFLD (odds ratio [OR] 1.17 [95% CI 1.05-1.3], pz = 0.003) in Caucasian adults. The variant was also positively associated with presence of advanced fibrosis (OR 1.22 [95% CI 1.03-1.45], pz = 0.021) in Caucasian adults using a recessive model of inheritance (CC + CT vs. TT). Meta-analysis of data from previous GWAS found the variant to be associated with higher ALT (pz = 0.002) and lower serum triglycerides (pz = 1.5x10(-4)). rs641738C>T was not associated with fasting insulin and no effect was observed in children with NAFLD. CONCLUSIONS: Our study validates rs641738C>T near MBOAT7 as a risk factor for the presence and severity of NAFLD in individuals of European descent. LAY SUMMARY: Fatty liver disease is a common condition where fat builds up in the liver, which can cause liver inflammation and scarring (including 'cirrhosis'). It is closely linked to obesity and diabetes, but some genes are also thought to be important. We did this study to see whether one specific change ('variant') in one gene ('MBOAT7') was linked to fatty liver disease. We took data from over 40 published studies and found that this variant near MBOAT7 is linked to more severe fatty liver disease. This means that drugs designed to work on MBOAT7 could be useful for treating fatty liver disease.

Authors: K. Teo, K. W. M. Abeysekera, L. Adams, E. Aigner, Q. M. Anstee, J. M. Banales, R. Banerjee, P. Basu, T. Berg, P. Bhatnagar, S. Buch, A. Canbay, S. Caprio, A. Chatterjee, Y. D. Ida Chen, A. Chowdhury, A. K. Daly, C. Datz, D. de Gracia Hahn, J. K. DiStefano, J. Dong, A. Duret, C. Emdin, M. Fairey, G. S. Gerhard, X. Guo, J. Hampe, M. Hickman, L. Heintz, C. Hudert, H. Hunter, M. Kelly, J. Kozlitina, M. Krawczyk, F. Lammert, C. Langenberg, J. Lavine, L. Li, H. K. Lim, R. Loomba, P. K. Luukkonen, P. E. Melton, T. A. Mori, N. D. Palmer, C. A. Parisinos, S. G. Pillai, F. Qayyum, M. C. Reichert, S. Romeo, J. I. Rotter, Y. R. Im, N. Santoro, C. Schafmayer, E. K. Speliotes, S. Stender, F. Stickel, C. D. Still, P. Strnad, K. D. Taylor, A. Tybjaerg-Hansen, G. R. Umano, M. Utukuri, L. Valenti, L. E. Wagenknecht, N. J. Wareham, R. M. Watanabe, J. Wattacheril, H. Yaghootkar, H. Yki-Jarvinen, K. A. Young, J. P. Mann

Date Published: 4th Sep 2020

Publication Type: Journal

PubMed ID: 32882372

Citation: J Hepatol. 2021 Jan;74(1):20-30. doi: 10.1016/j.jhep.2020.08.027. Epub 2020 Aug 31.

Created: 30th Jun 2021 at 13:06, Last updated: 8th Mar 2024 at 07:44

rs641738C>T near MBOAT7 is associated with liver fat, ALT, and fibrosis in NAFLD: a meta-analysis.

LiSyM Pillar I: Early Metabolic Injury (LiSyM-EMI)

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BACKGROUND & AIMS: A common genetic variant near MBOAT7 (rs641738C>T) has been previously associated with hepatic fat and advanced histology in non-alcoholic fatty liver disease (NAFLD), however, …

Date Published: 31st Aug 2020

Publication Type: Journal

PubMed ID: 32882372

Citation: J Hepatol. 2020 Aug 31. pii: S0168-8278(20)33598-4. doi: 10.1016/j.jhep.2020.08.027.

Created: 29th Sep 2020 at 12:47, Last updated: 8th Mar 2024 at 07:44

Volume-Function Analysis (LiMAx Test) in Patients with HCC and Cirrhosis Undergoing TACE-A Feasibility Study.

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

Abstract (Expand)

BACKGROUND: Transarterial chemoembolization (TACE) is an important therapy for hepatocellular carcinoma (HCC) in cirrhosis. In particular in advanced cirrhosis, post-TACE hepatic failure liver (PTHF) …

Authors: M. C. Reichert, A. Massmann, A. Schulz, A. Buecker, M. Glanemann, F. Lammert, M. Malinowski

Date Published: 21st Aug 2020

Publication Type: Journal

PubMed ID: 32816218

Citation: Dig Dis Sci. 2021 Jul;66(7):2452-2460. doi: 10.1007/s10620-020-06535-5. Epub 2020 Aug 20.

Created: 30th Jun 2021 at 08:43, Last updated: 8th Mar 2024 at 07:44

Predictive Power of Liver Maximum Function Capacity Test in Transjugular Intrahepatic Portosystemic Shunt Patients: A Pilot Study.

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

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BACKGROUND: Transjugular intrahepatic shunt (TIPSS) is placed in patients with variceal bleeding, refractory ascites, and for other indications. Postprocedural liver function-associated complications …

Authors: M. C. Reichert, A. Schulz, A. Massmann, A. Buecker, M. Glanemann, F. Lammert, M. Malinowski

Date Published: 17th Oct 2019

Publication Type: Journal

PubMed ID: 31618751

Citation: Dig Dis. 2020;38(3):251-258. doi: 10.1159/000503098. Epub 2019 Oct 16.

Created: 30th Jun 2021 at 08:42, 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

Date Published: 24th May 2019

Publication Type: Not specified

PubMed ID: 31121167

Citation: Gastroenterology. 2019 Sep;157(3):705-719.e18. doi: 10.1053/j.gastro.2019.05.013. Epub 2019 May 20.

Created: 8th Jun 2020 at 06:35, Last updated: 8th Mar 2024 at 07:44

Common NOD2 Risk Variants as Major Susceptibility Factors for Bacterial Infections in Compensated Cirrhosis.

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

Abstract (Expand)

OBJECTIVES: Common nucleotide-binding oligomerization domain containing 2 (NOD2) gene variants have been associated with bacterial infections (BIs) in cirrhosis, in particular, spontaneous bacterial …

Authors: M. C. Reichert, C. Ripoll, M. Casper, R. Greinert, E. Vandieken, F. Grunhage, B. Appenrodt, A. Zipprich, F. Lammert

Date Published: 1st Feb 2019

Publication Type: Not specified

PubMed ID: 30702490

Citation: Clin Transl Gastroenterol. 2019 Jan;10(1):e00002. doi: 10.14309/ctg.0000000000000002.

Created: 27th Jun 2019 at 07:01, Last updated: 8th Mar 2024 at 07:44

ABCB4 Gene Aberrations in Human Liver Disease: An Evolving Spectrum

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

Abstract

Not specified

Authors: Matthias Reichert, Frank Lammert

Date Published: 24th Oct 2018

Publication Type: Not specified

DOI: 10.1055/s-0038-1667299

Citation: Semin Liver Dis 38(04) : 299

Created: 13th Dec 2018 at 12:53, Last updated: 8th Mar 2024 at 07:44

Heterozygous carriage of the alpha1-antitrypsin Pi*Z variant increases the risk to develop liver cirrhosis.

LiSyM Pillar I: Early Metabolic Injury (LiSyM-EMI)

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Abstract (Expand)

OBJECTIVE: Homozygous alpha1-antitrypsin (AAT) deficiency increases the risk for developing cirrhosis, whereas the relevance of heterozygous carriage remains unclear. Hence, we evaluated the impact of …

Authors: P. Strnad, S. Buch, K. Hamesch, J. Fischer, J. Rosendahl, R. Schmelz, S. Brueckner, M. Brosch, C. V. Heimes, V. Woditsch, D. Scholten, H. D. Nischalke, S. Janciauskiene, M. Mandorfer, M. Trauner, M. J. Way, A. McQuillin, M. C. Reichert, M. Krawczyk, M. Casper, F. Lammert, F. Braun, W. von Schonfels, S. Hinz, G. Burmeister, C. Hellerbrand, A. Teufel, A. Feldman, J. M. Schattenberg, H. Bantel, A. Pathil, M. Demir, J. Kluwe, T. Boettler, M. Ridinger, N. Wodarz, M. Soyka, M. Rietschel, F. Kiefer, T. Weber, S. Marhenke, A. Vogel, H. Hinrichsen, A. Canbay, M. Schlattjan, K. Sosnowsky, C. Sarrazin, J. von Felden, A. Geier, P. Deltenre, B. Sipos, C. Schafmayer, M. Nothnagel, E. Aigner, C. Datz, F. Stickel, M. Y. Morgan, J. Hampe, T. Berg, C. Trautwein

Date Published: 3rd Aug 2018

Publication Type: Journal

PubMed ID: 30068662

Citation: Gut. 2019 Jun;68(6):1099-1107. doi: 10.1136/gutjnl-2018-316228. Epub 2018 Aug 1.

Created: 29th Sep 2020 at 12:54, Last updated: 8th Mar 2024 at 07:44

Genetic determinants of cholangiopathies: Molecular and systems genetics.

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

Abstract (Expand)

Familial cholangiopathies are rare but potentially severe diseases. Their spectrum ranges from fairly benign conditions as, for example, benign recurrent intrahepatic cholestasis to low-phospholipid …

Authors: M. C. Reichert, R. A. Hall, M. Krawczyk, F. Lammert

Date Published: 2nd Aug 2017

Publication Type: Journal

PubMed ID: 28757171

Citation: Biochim Biophys Acta Mol Basis Dis. 2018 Apr;1864(4 Pt B):1484-1490. doi: 10.1016/j.bbadis.2017.07.029. Epub 2017 Jul 27.

Created: 30th Jun 2021 at 08:47, Last updated: 8th Mar 2024 at 07:44

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