Zeisberg, Elisabeth M.

[["dc.bibliographiccitation.artnumber","16"],["dc.bibliographiccitation.issue","1"],["dc.bibliographiccitation.journal","Fibrogenesis & Tissue Repair"],["dc.bibliographiccitation.volume","8"],["dc.contributor.author","Zeisberg, Michael"],["dc.contributor.author","Zeisberg, Elisabeth M."],["dc.date.accessioned","2019-07-09T11:41:46Z"],["dc.date.available","2019-07-09T11:41:46Z"],["dc.date.issued","2015"],["dc.description.abstract","Based on extensive pre-clinical achievements over the past decades, it appears to be due time for a successful clinical translation in the renal fibrosis field—but what is the quickest road to get there? In light of the recent launch of the Precision Medicine Initiative and success of molecularly informed drugs in oncology, we here discuss what it may take to bring molecularly targeted anti-fibrotic to clinical use in chronic progressive kidney disease."],["dc.identifier.doi","10.1186/s13069-015-0033-x"],["dc.identifier.pmid","26330891"],["dc.identifier.purl","https://resolver.sub.uni-goettingen.de/purl?gs-1/12332"],["dc.identifier.uri","https://resolver.sub.uni-goettingen.de/purl?gro-2/58506"],["dc.language.iso","en"],["dc.notes.intern","Merged from goescholar"],["dc.rights","CC BY 4.0"],["dc.rights.uri","https://creativecommons.org/licenses/by/4.0"],["dc.title","Precision renal medicine: a roadmap towards targeted kidney fibrosis therapies"],["dc.type","journal_article"],["dc.type.internalPublication","yes"],["dc.type.version","published_version"],["dspace.entity.type","Publication"]]

[["dc.bibliographiccitation.journal","Open Journal of Bioresources"],["dc.bibliographiccitation.volume","7"],["dc.contributor.author","Beuthner, Bo E. C."],["dc.contributor.author","Topci, Rodi"],["dc.contributor.author","Derks, Mareike"],["dc.contributor.author","Franke, Thomas"],["dc.contributor.author","Seelke, Sandra"],["dc.contributor.author","Puls, Miriam"],["dc.contributor.author","Schuster, Andreas"],["dc.contributor.author","Toischer, Karl"],["dc.contributor.author","Valentova, Miroslava"],["dc.contributor.author","Cyganek, Lukas"],["dc.contributor.author","Zeisberg, Elisabeth M."],["dc.contributor.author","Jacobshagen, Claudius"],["dc.contributor.author","Hasenfuss, Gerd"],["dc.contributor.author","Nußbeck, Sara Y."],["dc.date.accessioned","2020-06-16T13:21:23Z"],["dc.date.available","2020-06-16T13:21:23Z"],["dc.date.issued","2020"],["dc.description.abstract","The bioresource (>265 patients with >27,600 biospecimens until December 2019; recruitment ongoing) on severe aortic stenosis is of vital importance to improve the still incomplete understanding of its etiology as well as its transition to heart failure. The bioresource contains various biospecimens, standardised clinical and imaging data sets including transthoracic echocardiography, computed tomography and magnetic resonance imaging of the heart. Biospecimen sampling follows the SOP-driven collection scheme of the German Center for Cardiovascular Research (DZHK) for venous blood and urine [1]. In addition, left-ventricular endomyocardial biopsies, rectal swabs and skin biopsies (for subsequent generation of induced pluripotent stem cells) are collected. Data management includes the use of a professional biospecimen management system as well as a Picture Archiving and Communication System (PACS) for imaging data. A Good Clinical Practice (GCP)-conform software for the management of clinical data and a trusted third party for the management of patient identifying data and pseudonyms are in place. Given these conditions, there is a high reuse-potential for biospecimens and data."],["dc.identifier.doi","10.5334/ojb.65"],["dc.identifier.uri","https://resolver.sub.uni-goettingen.de/purl?gro-2/66366"],["dc.identifier.url","https://sfb1002.med.uni-goettingen.de/production/literature/publications/340"],["dc.language.iso","en"],["dc.relation","SFB 1002: Modulatorische Einheiten bei Herzinsuffizienz"],["dc.relation","SFB 1002 | D01: Erholung aus der Herzinsuffizienz – Einfluss von Fibrose und Transkriptionssignatur"],["dc.relation","SFB 1002 | INF: Unterstützung der SFB 1002 Forschungsdatenintegration, -visualisierung und -nachnutzung"],["dc.relation.issn","2056-5542"],["dc.relation.workinggroup","RG Cyganek (Stem Cell Unit)"],["dc.relation.workinggroup","RG E. Zeisberg (Kardiales Stroma)"],["dc.relation.workinggroup","RG Hasenfuß (Transition zur Herzinsuffizienz)"],["dc.relation.workinggroup","RG Nußbeck"],["dc.relation.workinggroup","RG Toischer (Kardiales Remodeling)"],["dc.rights","CC BY 3.0"],["dc.title","Interdisciplinary Research on Aortic Valve Stenosis: A Longitudinal Collection of Biospecimens and Clinical Data of Patients Undergoing Transcatheter Aortic Valve Replacement"],["dc.type","journal_article"],["dc.type.internalPublication","yes"],["dc.type.subtype","original_ja"],["dc.type.version","published_version"],["dspace.entity.type","Publication"]]

[["dc.bibliographiccitation.artnumber","13"],["dc.bibliographiccitation.firstpage","1"],["dc.bibliographiccitation.journal","Fibrogenesis & Tissue Repair"],["dc.bibliographiccitation.lastpage","10"],["dc.bibliographiccitation.volume","8"],["dc.contributor.author","Charytan, David M."],["dc.contributor.author","Cinelli, Angeles"],["dc.contributor.author","Zeisberg, Elisabeth M."],["dc.date.accessioned","2019-02-27T17:04:19Z"],["dc.date.available","2019-02-27T17:04:19Z"],["dc.date.issued","2015"],["dc.description.abstract","Background Chronic kidney disease (CKD) is an independent risk factor for the development and severity of coronary artery disease (CHD) and endothelial dysfunction. There is an increase in the circulating angiogenesis inhibitors endostatin (END), thrombospondin-2 (TSP), angiopoietin-2 (ANG) and the nitric oxide (NO) inhibitor asymmetric dimethyl arginine (ADMA) in CKD patients. The aim of this study was to evaluate associations of the serum level of these factors and of the related angiogenesis inhibitor, endoglin (ENG), with burden of coronary atherosclerosis. Methods One hundred twenty-two patients undergoing coronary angiography were recruited from the cardiac catheterization lab at a single center. The total burden of coronary plaque (mm2) and the presence of coronary collaterals were quantified using quantitative coronary angiography (QCA). Serum levels of angiogenesis inhibitors were measured by ELISA (ENG, END, and ANG), Luminex assay (TSP), or HLPC (ADMA), respectively. Associations with plaque burden and coronary collateral supply were analyzed in multi-variable linear and logistic regression models. Results There was no significant association found between levels of circulating ADMA, ENG, END, ANG, or TSP and coronary plaque burden or collateral formation. Conclusions Our findings suggest that associations of circulating END, ENG, TSP, and ANG with cardiovascular mortality are unlikely to be mediated via direct effects on coronary plaque formation or by inhibition of collateral formation. Whether associations of these factors with mortality are mediated via local concentrations, myocardial tissue, or intra-plaque expression of these factors or by an effect on plaque vulnerability merits additional investigation."],["dc.identifier.doi","10.1186/s13069-015-0029-6"],["dc.identifier.pmid","26213574"],["dc.identifier.purl","https://resolver.sub.uni-goettingen.de/purl?gs-1/12295"],["dc.identifier.uri","https://resolver.sub.uni-goettingen.de/purl?gro-2/57657"],["dc.identifier.url","https://sfb1002.med.uni-goettingen.de/production/literature/publications/111"],["dc.language.iso","en"],["dc.notes.intern","Merged from goescholar"],["dc.notes.status","final"],["dc.relation","SFB 1002: Modulatorische Einheiten bei Herzinsuffizienz"],["dc.relation","SFB 1002 | C01: Epigenetische Kontrolle der Herzfibrose"],["dc.relation.issn","1755-1536"],["dc.relation.workinggroup","RG E. Zeisberg (Kardiales Stroma)"],["dc.rights","CC BY 4.0"],["dc.rights.uri","https://creativecommons.org/licenses/by/4.0"],["dc.title","Association of circulating angiogenesis inhibitors and asymmetric dimethyl arginine with coronary plaque burden"],["dc.type","journal_article"],["dc.type.internalPublication","unknown"],["dc.type.subtype","original_ja"],["dc.type.version","published_version"],["dspace.entity.type","Publication"]]

[["dc.bibliographiccitation.artnumber","3509"],["dc.bibliographiccitation.firstpage","1"],["dc.bibliographiccitation.issue","1"],["dc.bibliographiccitation.journal","Nature Communications"],["dc.bibliographiccitation.lastpage","15"],["dc.bibliographiccitation.volume","9"],["dc.contributor.author","Xu, Xingbo"],["dc.contributor.author","Tan, Xiaoying"],["dc.contributor.author","Tampe, Björn"],["dc.contributor.author","Wilhelmi, Tim"],["dc.contributor.author","Hulshoff, Melanie S."],["dc.contributor.author","Saito, Shoji"],["dc.contributor.author","Moser, Tobias"],["dc.contributor.author","Kalluri, Raghu"],["dc.contributor.author","Hasenfuss, Gerd"],["dc.contributor.author","Zeisberg, Elisabeth M."],["dc.contributor.author","Zeisberg, Michael"],["dc.date.accessioned","2019-02-27T12:52:18Z"],["dc.date.available","2019-02-27T12:52:18Z"],["dc.date.issued","2018"],["dc.description.abstract","While suppression of specific genes through aberrant promoter methylation contributes to different diseases including organ fibrosis, gene-specific reactivation technology is not yet available for therapy. TET enzymes catalyze hydroxymethylation of methylated DNA, reactivating gene expression. We here report generation of a high-fidelity CRISPR/Cas9-based gene-specific dioxygenase by fusing an endonuclease deactivated high-fidelity Cas9 (dHFCas9) to TET3 catalytic domain (TET3CD), targeted to specific genes by guiding RNAs (sgRNA). We demonstrate use of this technology in four different anti-fibrotic genes in different cell types in vitro, among them RASAL1 and Klotho, both hypermethylated in kidney fibrosis. Furthermore, in vivo lentiviral delivery of the Rasal1-targeted fusion protein to interstitial cells and of the Klotho-targeted fusion protein to tubular epithelial cells each results in specific gene reactivation and attenuation of fibrosis, providing gene-specific demethylating technology in a disease model."],["dc.identifier.doi","10.1038/s41467-018-05766-5"],["dc.identifier.pmid","30158531"],["dc.identifier.purl","https://resolver.sub.uni-goettingen.de/purl?gs-1/15605"],["dc.identifier.uri","https://resolver.sub.uni-goettingen.de/purl?gro-2/57643"],["dc.identifier.url","https://sfb1002.med.uni-goettingen.de/production/literature/publications/225"],["dc.language.iso","en"],["dc.notes.intern","Merged from goescholar"],["dc.notes.status","final"],["dc.relation","SFB 1002: Modulatorische Einheiten bei Herzinsuffizienz"],["dc.relation","SFB 1002 | C01: Epigenetische Kontrolle der Herzfibrose"],["dc.relation","SFB 1002 | D03: ENPP3-vermittelter Phosphat-Metabolismus bei der Herzfibrose"],["dc.relation.issn","2041-1723"],["dc.relation.workinggroup","RG Hasenfuß (Transition zur Herzinsuffizienz)"],["dc.relation.workinggroup","RG E. Zeisberg (Kardiales Stroma)"],["dc.relation.workinggroup","RG M. Zeisberg (Renale Fibrogenese)"],["dc.rights","CC BY 4.0"],["dc.rights.uri","https://creativecommons.org/licenses/by/4.0"],["dc.title","High-fidelity CRISPR/Cas9- based gene-specific hydroxymethylation rescues gene expression and attenuates renal fibrosis"],["dc.type","journal_article"],["dc.type.internalPublication","unknown"],["dc.type.subtype","original_ja"],["dc.type.version","published_version"],["dspace.entity.type","Publication"]]

[["dc.bibliographiccitation.firstpage","19"],["dc.bibliographiccitation.issue","1"],["dc.bibliographiccitation.journal","EBioMedicine"],["dc.bibliographiccitation.lastpage","36"],["dc.bibliographiccitation.volume","2"],["dc.contributor.author","Tampe, Björn"],["dc.contributor.author","Tampe, Desiree"],["dc.contributor.author","Zeisberg, Elisabeth M."],["dc.contributor.author","Müller, Gerhard A."],["dc.contributor.author","Bechtel-Walz, Wibke"],["dc.contributor.author","Koziolek, Michael"],["dc.contributor.author","Kalluri, Raghu"],["dc.contributor.author","Zeisberg, Michael"],["dc.date.accessioned","2019-02-27T10:29:15Z"],["dc.date.available","2019-02-27T10:29:15Z"],["dc.date.issued","2015"],["dc.description.abstract","Progression of chronic kidney disease remains a principal problem in clinical nephrology and there is a pressing need for novel therapeutics and biomarkers. Aberrant promoter CpG island methylation and subsequent transcriptional silencing of specific genes have emerged as contributors to progression of chronic kidney disease. Here, we report that transcriptional silencing of the Ras-GTP suppressor RASAL1 contributes causally to progression of kidney fibrosis and we identified that circulating methylated RASAL1 promoter DNA fragments in peripheral blood correspond with levels of intrarenal levels of RASAL1 promoter methylation and degree of fibrosis in kidney biopsies, enabling non-invasive longitudinal analysis of intrarenal CpG island methylation. Retrospective analysis of patients with hypertensive nephrosclerosis revealed that circulating methylated RASAL1 promoter DNA fragments in peripheral blood decrease with Dihydralazine treatment in patients with hypertensive nephrosclerosis, and provided evidence that low-dose Dihydralazine delays decline of excretory kidney function, whereas Dihydralazine at standard doses had no protective effect. We demonstrate that the protective effect of Dihydralazine is due to induction of endogenous Tet3/Tdg-mediated DNA-de-methylation activity reversing aberrant promoter CpG island methylation, while HIF1α induction at standard doses counterbalances its protective activity. We conclude that RASAL1 promoter methylation is a therapeutic target and a biomarker of renal fibrosis. Our study suggests therapeutic use of low-dose Dihydralazine in patients with chronic kidney disease and fibrosis deserves further consideration."],["dc.identifier.doi","10.1016/j.ebiom.2014.11.005"],["dc.identifier.pmid","25717475"],["dc.identifier.purl","https://resolver.sub.uni-goettingen.de/purl?gs-1/11368"],["dc.identifier.uri","https://resolver.sub.uni-goettingen.de/purl?gro-2/57639"],["dc.identifier.url","https://sfb1002.med.uni-goettingen.de/production/literature/publications/62"],["dc.language.iso","en"],["dc.notes.intern","Merged from goescholar"],["dc.notes.status","final"],["dc.relation","SFB 1002: Modulatorische Einheiten bei Herzinsuffizienz"],["dc.relation","SFB 1002 | C01: Epigenetische Kontrolle der Herzfibrose"],["dc.relation.issn","2352-3964"],["dc.relation.workinggroup","RG E. Zeisberg (Kardiales Stroma)"],["dc.relation.workinggroup","RG M. Zeisberg (Renale Fibrogenese)"],["dc.rights","CC BY 3.0"],["dc.rights.uri","https://creativecommons.org/licenses/by/3.0"],["dc.title","Induction of Tet3-dependent Epigenetic Remodeling by Low-dose Hydralazine Attenuates Progression of Chronic Kidney Disease"],["dc.type","journal_article"],["dc.type.internalPublication","unknown"],["dc.type.subtype","original_ja"],["dc.type.version","published_version"],["dspace.entity.type","Publication"]]

[["dc.bibliographiccitation.artnumber","339"],["dc.bibliographiccitation.journal","BMC Musculoskeletal Disorders"],["dc.bibliographiccitation.volume","17"],["dc.contributor.author","Patschan, Susann A."],["dc.contributor.author","Tampe, Desiree"],["dc.contributor.author","Mueller, C."],["dc.contributor.author","Seitz, C."],["dc.contributor.author","Herink, Claudia"],["dc.contributor.author","Mueller, Georg Anton"],["dc.contributor.author","Zeisberg, Elisabeth M."],["dc.contributor.author","Zeisberg, Michael"],["dc.contributor.author","Henze, Elvira"],["dc.contributor.author","Patschan, Daniel"],["dc.date.accessioned","2018-11-07T10:10:11Z"],["dc.date.available","2018-11-07T10:10:11Z"],["dc.date.issued","2016"],["dc.description.abstract","Background: Patients with systemic sclerosis (SSc) are endagered by tissue fibrosis and by microvasculopathy, with the latter caused by endothelial cell expansion/proliferation. SSc-associated fibrosis potentially results from mesenchymal transdifferentiation of endothelial cells. Early Endothelial Progenitor Cells (eEPCs) act proangiogenic under diverse conditions. Aim of the study was to analyze eEPC regeneration and mesenchymal transdifferentiation in patients with limited and diffuse SSs (lSSc and dSSc). Methods: Patients with both, lSSc and dSSc were included into the study. The following parameters were evaluated: eEPC numbers and regeneration, concentrations of vasomodulatory mediators, mesenchymal properties of blood-derived eEPC. Serum samples of healthy subjects and SS patients were used for stimulation of cultured human eEPC, subsequently followed by analysis of mesenchymal cell characteristics and mobility. Results: Twenty-nine patients were included into the study. Regenerative activity of blood-derived eEPCs did not differ between Controls and patients. Circulating eEPC were significantly lower in all patients with SSc, and in limited and diffuse SSc (lSSc/dSSc). Serum concentrations of promesenchymal TGF-b was elevated in all patients with SSc. Cultured mononuclear cells from SS patients displayed higher abundances of CD31 and of CD31 and aSMA combined. Finally, serum from SSc patients inhibited migration of cultured eEPCs and the cells showed lower sensitivity towards the endothelin antagonist Bosentan. Conclusions: The eEPC system, which represents an essential element of the endogenous vascular repair machinery is affected in SSc. The increased appearance of mesenchymal properties in eEPC may indicate that alterations of the cells potentially contribute to the accumulation of connective tissue and to vascular malfunction."],["dc.description.sponsorship","Heidenreich von-Siebold Programm"],["dc.identifier.doi","10.1186/s12891-016-1197-2"],["dc.identifier.isi","000395017600003"],["dc.identifier.pmid","27519706"],["dc.identifier.purl","https://resolver.sub.uni-goettingen.de/purl?gs-1/13866"],["dc.identifier.uri","https://resolver.sub.uni-goettingen.de/purl?gro-2/39808"],["dc.notes.intern","Merged from goescholar"],["dc.notes.status","zu prüfen"],["dc.notes.submitter","Najko"],["dc.publisher","Biomed Central Ltd"],["dc.relation.issn","1471-2474"],["dc.rights","CC BY 4.0"],["dc.rights.uri","https://creativecommons.org/licenses/by/4.0"],["dc.title","Early Endothelial Progenitor Cells (eEPCs) in systemic sclerosis (SSc) - dynamics of cellular regeneration and mesenchymal transdifferentiation"],["dc.type","journal_article"],["dc.type.internalPublication","yes"],["dc.type.peerReviewed","yes"],["dc.type.status","published"],["dc.type.version","published_version"],["dspace.entity.type","Publication"]]

[["dc.bibliographiccitation.artnumber","e0143783"],["dc.bibliographiccitation.issue","11"],["dc.bibliographiccitation.journal","PLoS ONE"],["dc.bibliographiccitation.volume","10"],["dc.contributor.author","Amanzada, Ahmad"],["dc.contributor.author","Reinhardt, Lars"],["dc.contributor.author","Fey, Dorothea"],["dc.contributor.author","Zeisberg, Elisabeth M."],["dc.contributor.author","Mihm, Sabine"],["dc.date.accessioned","2018-11-07T09:48:47Z"],["dc.date.available","2018-11-07T09:48:47Z"],["dc.date.issued","2015"],["dc.description.abstract","Genetic polymorphisms in the region of the interferon-lambda genes (IFNL) associate with clearance of hepatitis C virus (HCV) infection. One of these polymorphisms, IFNL4 rs368234815, determines loss or gain of function of the IFNL4 gene by frameshift variation. The very same and a second one, IFNL3 rs4803217, are supposed to impact the expression of IFNL3: while IFNL4 rs368234815 is suggested to modulate IFNL3 transcription, IFNL3 rs4803217 is thought to alter IFNL3 mRNA stability. The latter process is believed to be partially driven by an HCV-induced ectopic expression of myosin heavy chain genes 7B and 7 and their coexpressed microRNAs mir499 and mir208B. These ideas are evidenced by functional investigations on peripheral blood mononuclear and hepatoma cells in culture. Our study aimed at exploring IFNL3 gene expression in clinical samples, i.e., in ex vivo derived liver tissue from patients with chronic hepatitis C (n = 57) and various other diseases (n = 56). By applying an assay designed to specifically quantify IFNL3 and discriminating paralogous IFNL2 transcripts, IFNL3 mRNA expression was not found to differ significantly between chronic hepatitis C and control samples. Among patients with chronic HCV infection, moreover, IFNL3 rs4803217 or IFNL4 rs368234815 minor alleles did not associate with reduced IFNL3 gene expression. Finally, myosin heavy chain genes 7B and 7 and corresponding microRNAs mir499 and mir208B were not found activated in liver in chronic HCV infection. Of note, detectability of MYH7 mRNA related to the procedure of liver biopsy sampling, as tissue obtained by direct punctation of the liver during laparoscopic inspection was less likely to contain MYH7 transcripts than samples acquired by percutaneous punctation. In conclusion, data on ex vivo derived liver tissue samples argue against an attenuating impact of IFNL3 rs4803217 or IFNL4 rs368234815 minor alleles on hepatic IFNL3 gene expression in vivo."],["dc.description.sponsorship","Deutsche Forschungsgemeinschaft (DFG) [MI 474/1-1]"],["dc.description.sponsorship","Open-Access Publikationsfonds 2015"],["dc.identifier.doi","10.1371/journal.pone.0143783"],["dc.identifier.isi","000365865300111"],["dc.identifier.pmid","26606750"],["dc.identifier.purl","https://resolver.sub.uni-goettingen.de/purl?gs-1/12614"],["dc.identifier.uri","https://resolver.sub.uni-goettingen.de/purl?gro-2/35377"],["dc.identifier.url","https://sfb1002.med.uni-goettingen.de/production/literature/publications/139"],["dc.notes.intern","Merged from goescholar"],["dc.notes.status","zu prüfen"],["dc.notes.submitter","Najko"],["dc.relation","SFB 1002: Modulatorische Einheiten bei Herzinsuffizienz"],["dc.relation","SFB 1002 | C01: Epigenetische Kontrolle der Herzfibrose"],["dc.relation.issn","1932-6203"],["dc.relation.workinggroup","RG E. Zeisberg (Kardiales Stroma)"],["dc.rights","CC BY 4.0"],["dc.rights.uri","https://creativecommons.org/licenses/by/4.0"],["dc.title","Hepatic Interferon-lambda 3 (IFNL3) Gene Expression Reveals Not to Be Attenuated in Non-Favorable IFNL3 rs4803217 or IFNL4 rs368234815 Minor Allele Carriers in Chronic Hepatitis C"],["dc.type","journal_article"],["dc.type.internalPublication","yes"],["dc.type.peerReviewed","yes"],["dc.type.subtype","original_ja"],["dc.type.version","published_version"],["dspace.entity.type","Publication"]]

[["dc.bibliographiccitation.firstpage","46"],["dc.bibliographiccitation.issue","1"],["dc.bibliographiccitation.journal","Journal of Cardiovascular Magnetic Resonance"],["dc.bibliographiccitation.volume","22"],["dc.contributor.author","Backhaus, Sören Jan"],["dc.contributor.author","Lange, Torben"],["dc.contributor.author","Beuthner, Bo Eric"],["dc.contributor.author","Topci, Rodi"],["dc.contributor.author","Wang, Xiaoqing"],["dc.contributor.author","Kowallick, Johannes Tammo"],["dc.contributor.author","Lotz, Joachim"],["dc.contributor.author","Seidler, Tim"],["dc.contributor.author","Toischer, Karl"],["dc.contributor.author","Zeisberg, Elisabeth M."],["dc.contributor.author","Puls, Miriam"],["dc.contributor.author","Jacobshagen, Claudius"],["dc.contributor.author","Uecker, Martin"],["dc.contributor.author","Hasenfuß, Gerd P."],["dc.contributor.author","Schuster, Andreas"],["dc.date.accessioned","2021-03-08T07:13:57Z"],["dc.date.available","2021-03-08T07:13:57Z"],["dc.date.issued","2020"],["dc.description.abstract","Myocardial fibrosis is a major determinant of outcome in aortic stenosis (AS). Novel fast real-time (RT) cardiovascular magnetic resonance (CMR) mapping techniques allow comprehensive quantification of fibrosis but have not yet been compared against standard techniques and histology."],["dc.identifier.doi","10.1186/s12968-020-00632-0"],["dc.identifier.pmid","32564773"],["dc.identifier.purl","https://resolver.sub.uni-goettingen.de/purl?gs-1/17418"],["dc.identifier.uri","https://resolver.sub.uni-goettingen.de/purl?gro-2/80477"],["dc.identifier.url","https://mbexc.uni-goettingen.de/literature/publications/50"],["dc.identifier.url","https://sfb1002.med.uni-goettingen.de/production/literature/publications/359"],["dc.language.iso","en"],["dc.notes.intern","Merged from goescholar"],["dc.relation","EXC 2067: Multiscale Bioimaging"],["dc.relation","SFB 1002: Modulatorische Einheiten bei Herzinsuffizienz"],["dc.relation","SFB 1002 | D01: Erholung aus der Herzinsuffizienz – Einfluss von Fibrose und Transkriptionssignatur"],["dc.relation.issn","1532-429X"],["dc.relation.workinggroup","RG Hasenfuß"],["dc.relation.workinggroup","RG Uecker"],["dc.relation.workinggroup","RG E. Zeisberg (Kardiales Stroma)"],["dc.relation.workinggroup","RG Backhaus"],["dc.relation.workinggroup","RG Toischer (Kardiales Remodeling)"],["dc.rights","CC BY 4.0"],["dc.rights.uri","https://creativecommons.org/licenses/by/4.0"],["dc.title","Real-time cardiovascular magnetic resonance T1 and extracellular volume fraction mapping for tissue characterisation in aortic stenosis"],["dc.type","journal_article"],["dc.type.internalPublication","yes"],["dc.type.subtype","original_ja"],["dc.type.version","published_version"],["dspace.entity.type","Publication"]]

[["dc.bibliographiccitation.firstpage","1903"],["dc.bibliographiccitation.issue","20"],["dc.bibliographiccitation.journal","European Heart Journal"],["dc.bibliographiccitation.lastpage","1914"],["dc.bibliographiccitation.volume","41"],["dc.contributor.author","Puls, Miriam"],["dc.contributor.author","Beuthner, Bo Eric"],["dc.contributor.author","Topci, Rodi"],["dc.contributor.author","Vogelgesang, Anja"],["dc.contributor.author","Bleckmann, Annalen"],["dc.contributor.author","Sitte, Maren"],["dc.contributor.author","Lange, Torben"],["dc.contributor.author","Backhaus, Sören Jan"],["dc.contributor.author","Schuster, Andreas"],["dc.contributor.author","Seidler, Tim"],["dc.contributor.author","Kutschka, Ingo"],["dc.contributor.author","Toischer, Karl"],["dc.contributor.author","Zeisberg, Elisabeth Maria"],["dc.contributor.author","Jacobshagen, Claudius"],["dc.contributor.author","Hasenfuß, Gerd"],["dc.date.accessioned","2020-06-16T13:21:30Z"],["dc.date.available","2020-06-16T13:21:30Z"],["dc.date.issued","2020-05-21"],["dc.description.abstract","Myocardial fibrosis (MF) might represent a key player in pathophysiology of heart failure in aortic stenosis (AS). We aimed to assess its impact on left ventricular (LV) remodelling, recovery, and mortality after transcatheter aortic valve implantation (TAVI) in different AS subtypes."],["dc.identifier.doi","10.1093/eurheartj/ehaa033"],["dc.identifier.pmid","32049275"],["dc.identifier.uri","https://resolver.sub.uni-goettingen.de/purl?gro-2/66367"],["dc.identifier.url","https://mbexc.uni-goettingen.de/literature/publications/438"],["dc.identifier.url","https://sfb1002.med.uni-goettingen.de/production/literature/publications/341"],["dc.language.iso","en"],["dc.relation","EXC 2067: Multiscale Bioimaging"],["dc.relation","SFB 1002: Modulatorische Einheiten bei Herzinsuffizienz"],["dc.relation","SFB 1002 | D01: Erholung aus der Herzinsuffizienz – Einfluss von Fibrose und Transkriptionssignatur"],["dc.relation","SFB 1002 | D04: Bedeutung der Methylierung von RNA (m6A) und des Histons H3 (H3K4) in der Herzinsuffizienz"],["dc.relation","SFB 1002 | INF: Unterstützung der SFB 1002 Forschungsdatenintegration, -visualisierung und -nachnutzung"],["dc.relation.eissn","1522-9645"],["dc.relation.issn","0195-668X"],["dc.relation.workinggroup","RG Hasenfuß"],["dc.relation.workinggroup","RG E. Zeisberg (Kardiales Stroma)"],["dc.relation.workinggroup","RG Backhaus"],["dc.relation.workinggroup","RG Toischer (Kardiales Remodeling)"],["dc.rights","CC BY-NC 4.0"],["dc.title","Impact of myocardial fibrosis on left ventricular remodelling, recovery, and outcome after transcatheter aortic valve implantation in different haemodynamic subtypes of severe aortic stenosis"],["dc.type","journal_article"],["dc.type.internalPublication","yes"],["dc.type.subtype","original_ja"],["dc.type.version","published_version"],["dspace.entity.type","Publication"]]

[["dc.bibliographiccitation.artnumber","e0147816"],["dc.bibliographiccitation.firstpage","1"],["dc.bibliographiccitation.issue","1"],["dc.bibliographiccitation.journal","PLoS ONE"],["dc.bibliographiccitation.lastpage","17"],["dc.bibliographiccitation.volume","11"],["dc.contributor.author","Tan, Xiaoying"],["dc.contributor.author","Xu, Xingbo"],["dc.contributor.author","Zeisberg, Michael"],["dc.contributor.author","Zeisberg, Elisabeth M."],["dc.date.accessioned","2018-11-07T10:19:09Z"],["dc.date.available","2018-11-07T10:19:09Z"],["dc.date.issued","2016"],["dc.description.abstract","While phosphorus in the form of inorganic or organic phosphate is critically involved in most cellular functions, high plasma levels of inorganic phosphate levels have emerged as independent risk factor for cardiac fibrosis, cardiovascular morbidity and decreased life-expectancy. While the link of high phosphate and cardiovascular disease is commonly explained by direct cellular effects of phospho-regulatory hormones, we here explored the possibility of inorganic phosphate directly eliciting biological responses in cells. We demonstrate that human coronary endothelial cells (HCAEC) undergo an endothelial-mesenchymal transition (EndMT) when exposed to high phosphate. We further demonstrate that such EndMT is initiated by recruitment of aberrantly phosphorylated DNMT1 to the RASAL1 CpG island promoter by HDAC2, causing aberrant promoter methylation and transcriptional suppression, ultimately leading to increased Ras-GTP activity and activation of common EndMT regulators Twist and Snail. Our studies provide a novel aspect for known adverse effects of high phosphate levels, as eukaryotic cells are commonly believed to have lost phosphate-sensing mechanisms of prokaryotes during evolution, rendering them insensitive to extracellular inorganic orthophosphate. In addition, our studies provide novel insights into the mechanisms underlying specific targeting of select genes in context of fibrogenesis."],["dc.identifier.doi","10.1371/journal.pone.0147816"],["dc.identifier.isi","000369528200055"],["dc.identifier.pmid","26815200"],["dc.identifier.purl","https://resolver.sub.uni-goettingen.de/purl?gs-1/12846"],["dc.identifier.uri","https://resolver.sub.uni-goettingen.de/purl?gro-2/41608"],["dc.identifier.url","https://sfb1002.med.uni-goettingen.de/production/literature/publications/137"],["dc.language.iso","en"],["dc.notes.intern","Merged from goescholar"],["dc.notes.status","final"],["dc.notes.submitter","Najko"],["dc.relation","SFB 1002: Modulatorische Einheiten bei Herzinsuffizienz"],["dc.relation","SFB 1002 | C01: Epigenetische Kontrolle der Herzfibrose"],["dc.relation.issn","1932-6203"],["dc.relation.workinggroup","RG E. Zeisberg (Kardiales Stroma)"],["dc.relation.workinggroup","RG M. Zeisberg (Renale Fibrogenese)"],["dc.rights","CC BY 4.0"],["dc.rights.uri","https://creativecommons.org/licenses/by/4.0"],["dc.title","DNMT1 and HDAC2 Cooperate to Facilitate Aberrant Promoter Methylation in Inorganic Phosphate-Induced Endothelial-Mesenchymal Transition"],["dc.type","journal_article"],["dc.type.internalPublication","yes"],["dc.type.peerReviewed","yes"],["dc.type.subtype","original_ja"],["dc.type.version","published_version"],["dspace.entity.type","Publication"]]