Zeisberg, Elisabeth M.

[["dc.bibliographiccitation.firstpage","264"],["dc.bibliographiccitation.issue","2"],["dc.bibliographiccitation.journal","Journal of Pathology"],["dc.bibliographiccitation.lastpage","273"],["dc.bibliographiccitation.volume","229"],["dc.contributor.author","Zeisberg, Elisabeth M."],["dc.contributor.author","Zeisberg, Michael"],["dc.date.accessioned","2018-11-07T09:30:53Z"],["dc.date.accessioned","2019-02-19T16:44:38Z"],["dc.date.available","2018-11-07T09:30:53Z"],["dc.date.available","2019-02-19T16:44:38Z"],["dc.date.issued","2013"],["dc.description.abstract","The aberrant methylation of CpG island promoters of selected genes is the prominent epigenetic mechanism by which gene transcription can be effectively silenced. Aberrant hypermethylation of a few selected genes plays an important role in facilitating fibrotic fibroblast activation and in driving fibrogenesis. Here we review mechanisms of DNA methylation and demethylation and their implications for fibroblast activation and tissue fibrosis."],["dc.identifier.doi","10.1002/path.4120"],["dc.identifier.isi","000312542400013"],["dc.identifier.pmid","23097091"],["dc.identifier.uri","https://resolver.sub.uni-goettingen.de/purl?gro-2/31417"],["dc.identifier.uri","https://resolver.sub.uni-goettingen.de/purl?gro-2/57601"],["dc.identifier.url","https://sfb1002.med.uni-goettingen.de/production/literature/publications/78"],["dc.language.iso","en"],["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","0022-3417"],["dc.relation.issn","1096-9896"],["dc.relation.workinggroup","RG E. Zeisberg (Kardiales Stroma)"],["dc.relation.workinggroup","RG M. Zeisberg (Renale Fibrogenese)"],["dc.title","The role of promoter hypermethylation in fibroblast activation and fibrogenesis"],["dc.type","journal_article"],["dc.type.internalPublication","yes"],["dc.type.peerReviewed","yes"],["dc.type.subtype","overview_ja"],["dspace.entity.type","Publication"]]

[["dc.bibliographiccitation.firstpage","136"],["dc.bibliographiccitation.journal","Neurobiology of Learning and Memory"],["dc.bibliographiccitation.lastpage","150"],["dc.bibliographiccitation.volume","150"],["dc.contributor.author","Dere, Ekrem"],["dc.contributor.author","Ronnenberg, Anja"],["dc.contributor.author","Tampe, Björn"],["dc.contributor.author","Arinrad, Sahab"],["dc.contributor.author","Schmidt, Manuela"],["dc.contributor.author","Zeisberg, Elisabeth"],["dc.contributor.author","Ehrenreich, Hannelore"],["dc.date.accessioned","2020-12-10T15:20:34Z"],["dc.date.available","2020-12-10T15:20:34Z"],["dc.date.issued","2018"],["dc.identifier.doi","10.1016/j.nlm.2018.02.023"],["dc.identifier.issn","1074-7427"],["dc.identifier.uri","https://resolver.sub.uni-goettingen.de/purl?gro-2/72715"],["dc.language.iso","en"],["dc.notes.intern","DOI Import GROB-354"],["dc.title","Cognitive, emotional and social phenotyping of mice in an observer-independent setting"],["dc.type","journal_article"],["dc.type.internalPublication","yes"],["dspace.entity.type","Publication"]]

[["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","American Journal of Respiratory and Critical Care Medicine"],["dc.bibliographiccitation.volume","193"],["dc.contributor.author","Zuo, H."],["dc.contributor.author","Poppinga, W. J."],["dc.contributor.author","Zeisberg, Elisabeth M."],["dc.contributor.author","Nikolaev, V. O."],["dc.contributor.author","Schmidt, M."],["dc.date.accessioned","2018-11-07T10:19:43Z"],["dc.date.available","2018-11-07T10:19:43Z"],["dc.date.issued","2016"],["dc.identifier.isi","000390749605531"],["dc.identifier.uri","https://resolver.sub.uni-goettingen.de/purl?gro-2/41719"],["dc.notes.status","zu prüfen"],["dc.notes.submitter","Najko"],["dc.publisher","Amer Thoracic Soc"],["dc.publisher.place","New york"],["dc.relation.conference","International Conference of the American-Thoracic-Society (ATS)"],["dc.relation.eventlocation","San Francisco, CA"],["dc.title","Monitoring Local Pulmonary Camp Levels: Combining Precision Cut Lung Slice (pcls) And Fluorescence Resonance Energy Transfer (fret) Technologies In Mice"],["dc.type","conference_abstract"],["dc.type.internalPublication","yes"],["dc.type.peerReviewed","yes"],["dspace.entity.type","Publication"]]

[["dc.bibliographiccitation.firstpage","629"],["dc.bibliographiccitation.issue","6"],["dc.bibliographiccitation.journal","Seminars in nephrology"],["dc.bibliographiccitation.lastpage","636"],["dc.bibliographiccitation.volume","38"],["dc.contributor.author","Hulshoff, Melanie S."],["dc.contributor.author","Rath, Sandip K."],["dc.contributor.author","Xu, Xingbo"],["dc.contributor.author","Zeisberg, Michael"],["dc.contributor.author","Zeisberg, Elisabeth M."],["dc.date.accessioned","2020-11-24T12:13:03Z"],["dc.date.available","2020-11-24T12:13:03Z"],["dc.date.issued","2018"],["dc.description.abstract","Cardiovascular disease and heart failure are the primary cause of morbidity and mortality in patients with chronic kidney disease. Because impairment of kidney function correlates with heart failure and cardiac fibrosis, a kidney-heart axis is suspected. Although our understanding of the underlying mechanisms still is evolving, the possibility that kidney-heart messengers could be intercepted offers ample reason to focus on this clinically highly relevant problem. Here, we review the current knowledge of how kidney injury causes heart failure and fibrosis."],["dc.identifier.doi","10.1016/j.semnephrol.2018.08.007"],["dc.identifier.pmid","30413256"],["dc.identifier.uri","https://resolver.sub.uni-goettingen.de/purl?gro-2/69168"],["dc.language.iso","en"],["dc.relation.eissn","1558-4488"],["dc.relation.issn","0270-9295"],["dc.title","Causal Connections From Chronic Kidney Disease to Cardiac Fibrosis"],["dc.type","journal_article"],["dc.type.internalPublication","yes"],["dc.type.subtype","original_ja"],["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.firstpage","S18"],["dc.bibliographiccitation.journal","Der Internist"],["dc.bibliographiccitation.lastpage","S19"],["dc.bibliographiccitation.volume","57"],["dc.contributor.author","Alnour, Fouzi"],["dc.contributor.author","Xu, X."],["dc.contributor.author","Zeisberg, Michael"],["dc.contributor.author","Zeisberg, Elisabeth M."],["dc.date.accessioned","2018-11-07T10:15:49Z"],["dc.date.available","2018-11-07T10:15:49Z"],["dc.date.issued","2016"],["dc.identifier.isi","000375417500031"],["dc.identifier.uri","https://resolver.sub.uni-goettingen.de/purl?gro-2/40892"],["dc.notes.status","zu prüfen"],["dc.notes.submitter","Najko"],["dc.publisher","Springer"],["dc.publisher.place","New york"],["dc.relation.issn","1432-1289"],["dc.relation.issn","0020-9554"],["dc.title","KIAA0182: a new gene relevant for cardiac development"],["dc.type","conference_abstract"],["dc.type.internalPublication","yes"],["dc.type.peerReviewed","yes"],["dc.type.status","published"],["dspace.entity.type","Publication"]]

[["dc.bibliographiccitation.firstpage","2687"],["dc.bibliographiccitation.issue","10"],["dc.bibliographiccitation.journal","American Journal Of Pathology"],["dc.bibliographiccitation.lastpage","2698"],["dc.bibliographiccitation.volume","184"],["dc.contributor.author","Zeisberg, Michael"],["dc.contributor.author","Tampe, Bjoern"],["dc.contributor.author","LeBleu, Valerie S."],["dc.contributor.author","Tampe, Desiree"],["dc.contributor.author","Zeisberg, Elisabeth M."],["dc.contributor.author","Kalluri, Raghu"],["dc.date.accessioned","2018-11-07T09:34:44Z"],["dc.date.available","2018-11-07T09:34:44Z"],["dc.date.issued","2014"],["dc.description.abstract","Thrombospondin-1 (TSP1) is a multifunctional matricellular protein known to promote progression of chronic kidney disease. To gain insight into the underlying mechanisms through which TSP1 accelerates chronic kidney disease, we compared disease progression in Col4a3 knockout (K0) mice, which develop spontaneous kidney failure, with that of Col4a3;Tsp1 double-knockout (DK0) mice. Decline of excretory renal function was significantly delayed in the absence of TSP1. Although Col4a3;Tsp1 DK0 mice did progress toward end-stage renal failure, their kidneys exhibited distinct histopathological lesions, compared with creatinine level- matched Col4a3 K0 mice. Although kidneys of both Col4a3 K0 and Col4a3;Tsp1 DK0 mice exhibited a widened tubulointerstitium, predominant lesions in Col4a3 K0 kidneys were collagen deposition and fibroblast accumulation, whereas in Col4a3;Tsp1 DK0 kidney inflammation was predominant, with less collagen deposition. Altered disease progression correlated with impaired activation of transforming growth factor-beta 1 (TGF-beta 1) in vivo and in vitro in the absence of TSP1. In summary, our findings suggest that TSP1 contributes to progression of chronic kidney disease by catalyzing activation of latent TGF-beta 1, resulting in promotion of a fibroproliferative response over an inflammatory response. Furthermore, the findings suggest that fibro-proliferative and inflammatory lesions are independent entities, both of which contribute to decline of renal function."],["dc.identifier.doi","10.1016/j.ajpath.2014.06.014"],["dc.identifier.isi","000342276800010"],["dc.identifier.pmid","25111226"],["dc.identifier.uri","https://resolver.sub.uni-goettingen.de/purl?gro-2/32238"],["dc.identifier.url","https://sfb1002.med.uni-goettingen.de/production/literature/publications/79"],["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","1525-2191"],["dc.relation.issn","0002-9440"],["dc.relation.workinggroup","RG E. Zeisberg (Kardiales Stroma)"],["dc.relation.workinggroup","RG M. Zeisberg (Renale Fibrogenese)"],["dc.title","Thrombospondin-1 Deficiency Causes a Shift from Fibroproliferative to Inflammatory Kidney Disease and Delays Onset of Renal Failure"],["dc.type","journal_article"],["dc.type.internalPublication","yes"],["dc.type.peerReviewed","yes"],["dc.type.subtype","original_ja"],["dspace.entity.type","Publication"]]

[["dc.bibliographiccitation.firstpage","749"],["dc.bibliographiccitation.issue","9"],["dc.bibliographiccitation.journal","European heart journal"],["dc.bibliographiccitation.lastpage","758"],["dc.bibliographiccitation.volume","25"],["dc.contributor.author","Höcht-Zeisberg, Elisabeth"],["dc.contributor.author","Kahnert, H."],["dc.contributor.author","Guan, Kaomei"],["dc.contributor.author","Wulf, G"],["dc.contributor.author","Hemmerlein, Bernhard"],["dc.contributor.author","Schlott, T"],["dc.contributor.author","Tenderich, Gero"],["dc.contributor.author","Korfer, R."],["dc.contributor.author","Raute-Kreinsen, U."],["dc.contributor.author","Hasenfuß, Gerd"],["dc.date.accessioned","2017-09-07T11:43:25Z"],["dc.date.available","2017-09-07T11:43:25Z"],["dc.date.issued","2004"],["dc.description.abstract","Aims Recent studies have suggested that human extracardiac progenitor cells are capable of differentiating into cardiomyocytes. In animal studies, myocardial infarction attracted bone marrow stem cells and enhanced their differentiation into cardiomyocytes. Based on these findings, we hypothesised that myocardial infarction stimulates the invasion of progenitor cells and their differentiation into endothelial and cardiac cells in the human heart. Methods and results We compared autopsy samples from male control patients who had received a female donor heart with samples from such patients who developed myocardial infarction after transplantation. Fluorescence in situ hybridisation (FISH) for detection of the Y-chromosome was combined with immunofluorescence staining for CD45 and CD68 to distinguish host-derived inflammatory cells. Additionally, we used a 3D-confocal imaging technique to indisputably assign Y-chromosome-positive nuclei to their cytoplasm. In patients with myocardial infarction after heart transplantation (n = 5), host-derived non-inflammatory progenitor and endothelial cells were significantly increased compared to non-infarcted patients (n = 9). Yet, by using this novel multi-step approach, only 0.02% of all. cells were estimated to be mate cardiomyocytes and their increase in infarcted regions to 0.07% was not significant. Conclusion Myocardial infarction enhances the invasion of extracardiac progenitor cells and their regeneration of endothelial cells. However, a significant differentiation into cardiomyocytes as a physiological mechanism of postischaemic regeneration does not occur in transplanted patients. (C) 2004 The European Society of Cardiology. Published by Elsevier Ltd. All rights reserved."],["dc.identifier.doi","10.1016/j.ehj.2004.01.017"],["dc.identifier.gro","3143991"],["dc.identifier.isi","000221586800010"],["dc.identifier.pmid","15120885"],["dc.identifier.uri","https://resolver.sub.uni-goettingen.de/purl?gro-2/1565"],["dc.notes.intern","WoS Import 2017-03-10"],["dc.notes.status","final"],["dc.notes.submitter","PUB_WoS_Import"],["dc.publisher","W B Saunders Co Ltd"],["dc.relation.issn","0195-668X"],["dc.title","Cellular repopulation of myocardial infarction in patients with sex-mismatched heart transplantation"],["dc.type","journal_article"],["dc.type.internalPublication","yes"],["dc.type.peerReviewed","yes"],["dc.type.subtype","original"],["dspace.entity.type","Publication"]]

[["dc.bibliographiccitation.firstpage","75"],["dc.bibliographiccitation.issue","1"],["dc.bibliographiccitation.journal","Developmental Dynamics"],["dc.bibliographiccitation.lastpage","82"],["dc.bibliographiccitation.volume","237"],["dc.contributor.author","Tanjore, Harikrishna"],["dc.contributor.author","Zeisberg, Elisabeth M."],["dc.contributor.author","Gerami-Naini, Behzad"],["dc.contributor.author","Kalluri, Raghu"],["dc.date.accessioned","2022-03-01T11:45:29Z"],["dc.date.available","2022-03-01T11:45:29Z"],["dc.date.issued","2007"],["dc.identifier.doi","10.1002/dvdy.21385"],["dc.identifier.uri","https://resolver.sub.uni-goettingen.de/purl?gro-2/103346"],["dc.language.iso","en"],["dc.notes.intern","DOI-Import GROB-531"],["dc.relation.eissn","1097-0177"],["dc.relation.issn","1058-8388"],["dc.title","β1 integrin expression on endothelial cells is required for angiogenesis but not for vasculogenesis"],["dc.type","journal_article"],["dc.type.internalPublication","unknown"],["dspace.entity.type","Publication"]]