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.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.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"]]

[["dc.bibliographiccitation.firstpage","e23718"],["dc.bibliographiccitation.issue","8"],["dc.bibliographiccitation.journal","PLoS ONE"],["dc.bibliographiccitation.volume","6"],["dc.contributor.author","Charytan, David M."],["dc.contributor.author","Helfand, Alexander M."],["dc.contributor.author","MacDonald, Brian A."],["dc.contributor.author","Cinelli, Angeles"],["dc.contributor.author","Kalluri, Raghu"],["dc.contributor.author","Zeisberg, Elisabeth M."],["dc.contributor.editor","Charonis, Aristidis S."],["dc.date.accessioned","2022-03-01T11:44:10Z"],["dc.date.available","2022-03-01T11:44:10Z"],["dc.date.issued","2011"],["dc.identifier.doi","10.1371/journal.pone.0023718"],["dc.identifier.uri","https://resolver.sub.uni-goettingen.de/purl?gro-2/102950"],["dc.language.iso","en"],["dc.notes.intern","DOI-Import GROB-531"],["dc.relation.eissn","1932-6203"],["dc.rights.uri","http://creativecommons.org/licenses/by/4.0/"],["dc.title","Circulating Endoglin Concentration Is Not Elevated in Chronic Kidney Disease"],["dc.type","journal_article"],["dc.type.internalPublication","unknown"],["dspace.entity.type","Publication"]]

[["dc.bibliographiccitation.firstpage","157"],["dc.bibliographiccitation.issue","1"],["dc.bibliographiccitation.journal","Kidney International"],["dc.bibliographiccitation.lastpage","176"],["dc.bibliographiccitation.volume","91"],["dc.contributor.author","Tampe, Björn"],["dc.contributor.author","Steinle, Ulrike"],["dc.contributor.author","Tampe, Désirée"],["dc.contributor.author","Carstens, Julienne L."],["dc.contributor.author","Korsten, Peter"],["dc.contributor.author","Zeisberg, Elisabeth M."],["dc.contributor.author","Müller, Gerhard A."],["dc.contributor.author","Kalluri, Raghu"],["dc.contributor.author","Zeisberg, Michael"],["dc.date.accessioned","2020-05-04T07:22:12Z"],["dc.date.available","2020-05-04T07:22:12Z"],["dc.date.issued","2017"],["dc.description.abstract","Acute kidney injury (AKI) and progressive chronic kidney disease (CKD) are intrinsically tied syndromes. In this regard, the acutely injured kidney often does not achieve its full regenerative capacity and AKI directly transitions into progressive CKD associated with tubulointerstitial fibrosis. Underlying mechanisms of such AKI-to-CKD progression are still incompletely understood and specific therapeutic interventions are still elusive. Because epigenetic modifications play a role in maintaining tissue fibrosis, we used a murine model of ischemia-reperfusion injury to determine whether aberrant promoter methylation of RASAL1 contributes causally to the switch between physiological regeneration and tubulointerstitial fibrogenesis, a hallmark of AKI-to-CKD progression. It is known that the antihypertensive drug hydralazine has demethylating activity, and that its optimum demethylating activity occurs at concentrations below blood pressure-lowering doses. Administration of low-dose hydralazine effectively induced expression of hydroxylase TET3, which catalyzed RASAL1 hydroxymethylation and subsequent RASAL1 promoter demethylation. Hydralazine-induced CpG promoter demethylation subsequently attenuated renal fibrosis and preserved excretory renal function independent of its blood pressure-lowering effects. In comparison, RASAL1 demethylation and inhibition of tubulointerstitial fibrosis was not detected upon administration of the angiotensin-converting enzyme inhibitor Ramipril in this model. Thus, RASAL1 promoter methylation and subsequent transcriptional RASAL1 suppression plays a causal role in AKI-to-CKD progression."],["dc.identifier.doi","10.1016/j.kint.2016.07.042"],["dc.identifier.pmid","27692563"],["dc.identifier.uri","https://resolver.sub.uni-goettingen.de/purl?gro-2/64543"],["dc.identifier.url","https://sfb1002.med.uni-goettingen.de/production/literature/publications/307"],["dc.language.iso","en"],["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.eissn","1523-1755"],["dc.relation.issn","0085-2538"],["dc.relation.workinggroup","RG E. Zeisberg (Kardiales Stroma)"],["dc.relation.workinggroup","RG M. Zeisberg (Renale Fibrogenese)"],["dc.title","Low-dose hydralazine prevents fibrosis in a murine model of acute kidney injury-to-chronic kidney disease progression"],["dc.type","journal_article"],["dc.type.internalPublication","yes"],["dc.type.subtype","original_ja"],["dspace.entity.type","Publication"]]