Zeisberg, Elisabeth M.

[["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.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","1067"],["dc.bibliographiccitation.issue","6"],["dc.bibliographiccitation.journal","Renal Failure"],["dc.bibliographiccitation.lastpage","1069"],["dc.bibliographiccitation.volume","37"],["dc.contributor.author","Charytan, David M."],["dc.contributor.author","Padera, Robert F."],["dc.contributor.author","Helfand, Alexander M."],["dc.contributor.author","Zeisberg, Elisabeth M."],["dc.date.accessioned","2018-11-07T10:02:58Z"],["dc.date.available","2018-11-07T10:02:58Z"],["dc.date.issued","2015"],["dc.identifier.doi","10.3109/0886022X.2015.1040704"],["dc.identifier.isi","000361338600027"],["dc.identifier.pmid","25955707"],["dc.identifier.uri","https://resolver.sub.uni-goettingen.de/purl?gro-2/38341"],["dc.identifier.url","https://sfb1002.med.uni-goettingen.de/production/literature/publications/112"],["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","1525-6049"],["dc.relation.issn","0886-022X"],["dc.relation.workinggroup","RG E. Zeisberg (Kardiales Stroma)"],["dc.title","Association of activated vitamin D use with myocardial fibrosis and capillary supply: results of an autopsy study"],["dc.type","journal_article"],["dc.type.internalPublication","yes"],["dc.type.peerReviewed","yes"],["dc.type.subtype","original_ja"],["dspace.entity.type","Publication"]]

[["dc.bibliographiccitation.firstpage","113"],["dc.bibliographiccitation.journal","Journal of Molecular and Cellular Cardiology"],["dc.bibliographiccitation.lastpage","124"],["dc.bibliographiccitation.volume","136"],["dc.contributor.author","Liu, Qinghua"],["dc.contributor.author","Zhu, Lang-Jing"],["dc.contributor.author","Waaga-Gasser, Ana Maria"],["dc.contributor.author","Ding, Yan"],["dc.contributor.author","Cao, Minghua"],["dc.contributor.author","Jadhav, Shreyas J."],["dc.contributor.author","Kirollos, Sandra"],["dc.contributor.author","Shekar, Prem S."],["dc.contributor.author","Padera, Robert F."],["dc.contributor.author","Chang, Yu-Chun"],["dc.contributor.author","Xu, Xingbo"],["dc.contributor.author","Zeisberg, Elisabeth M."],["dc.contributor.author","Charytan, David M."],["dc.contributor.author","Hsiao, Li-Li"],["dc.date.accessioned","2020-12-10T15:21:48Z"],["dc.date.available","2020-12-10T15:21:48Z"],["dc.date.issued","2019"],["dc.identifier.doi","10.1016/j.yjmcc.2019.09.004"],["dc.identifier.issn","0022-2828"],["dc.identifier.purl","https://resolver.sub.uni-goettingen.de/purl?gs-1/16855"],["dc.identifier.uri","https://resolver.sub.uni-goettingen.de/purl?gro-2/73170"],["dc.language.iso","en"],["dc.notes.intern","DOI Import GROB-354"],["dc.notes.intern","Merged from goescholar"],["dc.rights","CC BY-NC-ND 4.0"],["dc.rights.uri","https://creativecommons.org/licenses/by-nc-nd/4.0"],["dc.title","The axis of local cardiac endogenous Klotho-TGF-β1-Wnt signaling mediates cardiac fibrosis in human"],["dc.type","journal_article"],["dc.type.internalPublication","yes"],["dc.type.version","published_version"],["dspace.entity.type","Publication"]]

[["dc.bibliographiccitation.firstpage","99"],["dc.bibliographiccitation.issue","1"],["dc.bibliographiccitation.journal","International Journal of Cardiology"],["dc.bibliographiccitation.lastpage","109"],["dc.bibliographiccitation.volume","176"],["dc.contributor.author","Charytan, David M."],["dc.contributor.author","Padera, Robert F."],["dc.contributor.author","Helfand, Alexander M."],["dc.contributor.author","Zeisberg, Michael"],["dc.contributor.author","Xu, X."],["dc.contributor.author","Liu, Xiaopeng"],["dc.contributor.author","Himmelfarb, Jonathan"],["dc.contributor.author","Cinelli, Angeles"],["dc.contributor.author","Kalluri, Raghu"],["dc.contributor.author","Zeisberg, Elisabeth M."],["dc.date.accessioned","2018-11-07T09:36:08Z"],["dc.date.available","2018-11-07T09:36:08Z"],["dc.date.issued","2014"],["dc.description.abstract","Background: Sudden cardiovascular death is increased in chronic kidney disease (CKD). Experimental CKD models suggest that angiogenesis and nitric oxide (NO) inhibitors induce myocardial fibrosis and microvascular dropout thereby facilitating arrhythmogenesis. We undertook this study to characterize associations of CKD with human myocardial pathology, NO-related circulating angiogenesis inhibitors, and endothelial cell behavior. Methods: We compared heart (n = 54) and serum (n = 162) samples from individuals with and without CKD, and assessed effects of serum on human coronary artery endothelial cells (HCAECs) in vitro. Left ventricular fibrosis and capillary density were quantified in post-mortem samples. Endothelial to mesenchymal transition (EndMT) was assessed by immunostaining of post-mortem samples and RNA expression in heart tissue obtained during cardiac surgery. Circulating asymmetric dimethylarginine (ADMA), endostatin (END), angiopoietin-2 (ANG), and thrombospondin-2 (TSP) were measured, and the effect of these factors and of subject serum on proliferation, apoptosis, and EndMT of HCAEC was analyzed. Results: Cardiac fibrosis increased 12% and 77% in stage 3-4 CKD and ESRD and microvascular density decreased 12% and 16% vs. preserved renal function. EndMT-derived fibroblast proportion was 17% higher in stage 3-4 CKD and ESRD (P-trend = 0.02). ADMA, ANG, TSP, and END concentrations increased in CKD. Both individual factors and CKD serum increased HCAEC apoptosis (P = 0.02), decreased proliferation (P = 0.03), and induced EndMT. Conclusions: CKD is associated with an increase in circulating angiogenesis and NO inhibitors, which impact proliferation and apoptosis of cardiac endothelial cells and promote EndMT, leading to cardiac fibrosis and capillary rarefaction. These processes may play key roles in CKD-associated CV disease. (C) 2014 Elsevier Ireland Ltd. All rights reserved."],["dc.identifier.doi","10.1016/j.ijcard.2014.06.062"],["dc.identifier.isi","000341040900026"],["dc.identifier.pmid","25049013"],["dc.identifier.uri","https://resolver.sub.uni-goettingen.de/purl?gro-2/32544"],["dc.identifier.url","https://sfb1002.med.uni-goettingen.de/production/literature/publications/6"],["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","1874-1754"],["dc.relation.issn","0167-5273"],["dc.relation.workinggroup","RG E. Zeisberg (Kardiales Stroma)"],["dc.relation.workinggroup","RG M. Zeisberg (Renale Fibrogenese)"],["dc.title","Increased concentration of circulating angiogenesis and nitric oxide inhibitors induces endothelial to mesenchymal transition and myocardial fibrosis in patients with chronic kidney disease"],["dc.type","journal_article"],["dc.type.internalPublication","yes"],["dc.type.peerReviewed","yes"],["dc.type.subtype","original_ja"],["dspace.entity.type","Publication"]]