Zeisberg, Elisabeth M.

[["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","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"]]

[["dc.bibliographiccitation.firstpage","2282"],["dc.bibliographiccitation.issue","12"],["dc.bibliographiccitation.journal","Journal of the American Society of Nephrology"],["dc.bibliographiccitation.lastpage","2287"],["dc.bibliographiccitation.volume","19"],["dc.contributor.author","Zeisberg, Elisabeth M."],["dc.contributor.author","Potenta, Scott E."],["dc.contributor.author","Sugimoto, Hikaru"],["dc.contributor.author","Zeisberg, Michael"],["dc.contributor.author","Kalluri, Raghu"],["dc.date.accessioned","2020-11-24T12:15:44Z"],["dc.date.available","2020-11-24T12:15:44Z"],["dc.date.issued","2008-12"],["dc.description.abstract","Fibroblasts are key mediators of fibrosis in the kidney and other organs, but their origin during fibrosis is still not completely clear. Activated fibroblasts likely arise from resident quiescent fibroblasts via epithelial-to-mesenchymal transition and from the bone marrow. Here, we demonstrate that endothelial cells also contribute to the emergence of fibroblasts during kidney fibrosis via the process of endothelial-to-mesenchymal transition (EndMT). We examined the contribution of EndMT to renal fibrosis in three mouse models of chronic kidney disease: (1) Unilateral ureteral obstructive nephropathy, (2) streptozotocin-induced diabetic nephropathy, and (3) a model of Alport renal disease. Approximately 30 to 50% of fibroblasts coexpressed the endothelial marker CD31 and markers of fibroblasts and myofibroblasts such as fibroblast specific protein-1 and alpha-smooth muscle actin. Endothelial lineage tracing using Tie2-Cre;R26R-stop-EYFP transgenic mice further confirmed the presence of EndMT-derived fibroblasts. Collectively, our results demonstrate that EndMT contributes to the accumulation of activated fibroblasts and myofibroblasts in kidney fibrosis and suggest that targeting EndMT might have therapeutic potential."],["dc.identifier.doi","10.1681/ASN.2008050513"],["dc.identifier.pmid","18987304"],["dc.identifier.uri","https://resolver.sub.uni-goettingen.de/purl?gro-2/69201"],["dc.language.iso","en"],["dc.relation.eissn","1533-3450"],["dc.relation.issn","1046-6673"],["dc.title","Fibroblasts in kidney fibrosis emerge via endothelial-to-mesenchymal transition"],["dc.type","journal_article"],["dc.type.internalPublication","unknown"],["dc.type.subtype","original_ja"],["dspace.entity.type","Publication"]]

[["dc.bibliographiccitation.firstpage","1304"],["dc.bibliographiccitation.issue","11"],["dc.bibliographiccitation.journal","Circulation Research"],["dc.bibliographiccitation.lastpage","1312"],["dc.bibliographiccitation.volume","107"],["dc.contributor.author","Zeisberg, Elisabeth M."],["dc.contributor.author","Kalluri, Raghu"],["dc.date.accessioned","2022-03-01T11:43:50Z"],["dc.date.available","2022-03-01T11:43:50Z"],["dc.date.issued","2010"],["dc.description.abstract","Cardiac fibroblasts play a critical role in maintenance of normal cardiac function. They are indispensable for damage control and tissue remodeling on myocardial injury and principal mediators of pathological cardiac remodeling and fibrosis. Despite their manyfold functions, cardiac fibroblasts remain poorly characterized in molecular terms. Evidence is evolving that cardiac fibroblasts are a heterogeneous population and likely derive from various distinct tissue niches in health and disease. Here, we review our emerging understanding of where cardiac fibroblasts come from, as well as how we can possibly use this knowledge to develop novel therapies for cardiac fibrosis."],["dc.description.abstract","Cardiac fibroblasts play a critical role in maintenance of normal cardiac function. They are indispensable for damage control and tissue remodeling on myocardial injury and principal mediators of pathological cardiac remodeling and fibrosis. Despite their manyfold functions, cardiac fibroblasts remain poorly characterized in molecular terms. Evidence is evolving that cardiac fibroblasts are a heterogeneous population and likely derive from various distinct tissue niches in health and disease. Here, we review our emerging understanding of where cardiac fibroblasts come from, as well as how we can possibly use this knowledge to develop novel therapies for cardiac fibrosis."],["dc.identifier.doi","10.1161/CIRCRESAHA.110.231910"],["dc.identifier.uri","https://resolver.sub.uni-goettingen.de/purl?gro-2/102853"],["dc.language.iso","en"],["dc.notes.intern","DOI-Import GROB-531"],["dc.relation.eissn","1524-4571"],["dc.relation.issn","0009-7330"],["dc.title","Origins of Cardiac Fibroblasts"],["dc.type","journal_article"],["dc.type.internalPublication","unknown"],["dspace.entity.type","Publication"]]

[["dc.bibliographiccitation.journal","European Journal of Heart Failure"],["dc.bibliographiccitation.volume","17"],["dc.contributor.author","Xu, X. X."],["dc.contributor.author","Tan, X."],["dc.contributor.author","Tampe, Bjoern"],["dc.contributor.author","Liu, X."],["dc.contributor.author","Maier, Lars S."],["dc.contributor.author","Sossalla, Samuel Tobias"],["dc.contributor.author","Kalluri, Raghu"],["dc.contributor.author","Zeisberg, Michael"],["dc.contributor.author","Hasenfuß, Gerd"],["dc.contributor.author","Zeisberg, Elisabeth M."],["dc.date.accessioned","2018-11-07T09:57:27Z"],["dc.date.available","2018-11-07T09:57:27Z"],["dc.date.issued","2015"],["dc.format.extent","373"],["dc.identifier.isi","000366200403437"],["dc.identifier.uri","https://resolver.sub.uni-goettingen.de/purl?gro-2/37161"],["dc.notes.status","zu prüfen"],["dc.notes.submitter","Najko"],["dc.publisher","Wiley-blackwell"],["dc.publisher.place","Hoboken"],["dc.relation.issn","1879-0844"],["dc.relation.issn","1388-9842"],["dc.title","Epigenetic balance of aberrant rasal1 promoter methylation and hydroxymethylation regulates cardiac fibrosis"],["dc.type","conference_abstract"],["dc.type.internalPublication","yes"],["dc.type.peerReviewed","yes"],["dc.type.status","published"],["dspace.entity.type","Publication"]]

[["dc.bibliographiccitation.firstpage","3053"],["dc.bibliographiccitation.issue","7"],["dc.bibliographiccitation.journal","The Journal of Clinical Investigation"],["dc.bibliographiccitation.lastpage","3070"],["dc.bibliographiccitation.volume","128"],["dc.contributor.author","Tampe, Björn"],["dc.contributor.author","Tampe, Désirée"],["dc.contributor.author","Nyamsuren, Gunsmaa"],["dc.contributor.author","Klöpper, Friederike"],["dc.contributor.author","Rapp, Gregor"],["dc.contributor.author","Kauffels, Anne"],["dc.contributor.author","Lorf, Thomas"],["dc.contributor.author","Zeisberg, Elisabeth M."],["dc.contributor.author","Müller, Gerhard A."],["dc.contributor.author","Kalluri, Raghu"],["dc.contributor.author","Hakroush, Samy"],["dc.contributor.author","Zeisberg, Michael"],["dc.date.accessioned","2020-12-10T18:38:19Z"],["dc.date.available","2020-12-10T18:38:19Z"],["dc.date.issued","2018"],["dc.description.abstract","Progression of chronic kidney disease associated with progressive fibrosis and impaired tubular epithelial regeneration is still an unmet biomedical challenge because, once chronic lesions have manifested, no effective therapies are available as of yet for clinical use. Prompted by various studies across multiple organs demonstrating that preconditioning regimens to induce endogenous regenerative mechanisms protect various organs from later incurring acute injuries, we here aimed to gain insights into the molecular mechanisms underlying successful protection and to explore whether such pathways could be utilized to inhibit progression of chronic organ injury. We identified a protective mechanism controlled by the transcription factor ARNT that effectively inhibits progression of chronic kidney injury by transcriptional induction of ALK3, the principal mediator of antifibrotic and proregenerative bone morphogenetic protein-signaling (BMP-signaling) responses. We further report that ARNT expression itself is controlled by the FKBP12/YY1 transcriptional repressor complex and that disruption of such FKBP12/YY1 complexes by picomolar FK506 at subimmunosuppressive doses increases ARNT expression, subsequently leading to homodimeric ARNT-induced ALK3 transcription. Direct targeting of FKBP12/YY1 with in vivo morpholino approaches or small molecule inhibitors, including GPI-1046, was equally effective for inducing ARNT expression, with subsequent activation of ALK3-dependent canonical BMP-signaling responses and attenuated chronic organ failure in models of chronic kidney disease, and also cardiac and liver injuries. In summary, we report an organ-protective mechanism that can be pharmacologically modulated by immunophilin ligands FK506 and GPI-1046 or therapeutically targeted by in vivo morpholino approaches."],["dc.identifier.doi","10.1172/JCI89632"],["dc.identifier.pmid","29664738"],["dc.identifier.uri","https://resolver.sub.uni-goettingen.de/purl?gro-2/77269"],["dc.identifier.url","https://sfb1002.med.uni-goettingen.de/production/literature/publications/308"],["dc.language.iso","en"],["dc.notes.intern","DOI Import GROB-354"],["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","1558-8238"],["dc.relation.issn","0021-9738"],["dc.relation.workinggroup","RG E. Zeisberg (Kardiales Stroma)"],["dc.relation.workinggroup","RG M. Zeisberg (Renale Fibrogenese)"],["dc.title","Pharmacological induction of hypoxia-inducible transcription factor ARNT attenuates chronic kidney failure"],["dc.type","journal_article"],["dc.type.internalPublication","yes"],["dc.type.subtype","original_ja"],["dspace.entity.type","Publication"]]

[["dc.bibliographiccitation.firstpage","952"],["dc.bibliographiccitation.issue","8"],["dc.bibliographiccitation.journal","Nature Medicine"],["dc.bibliographiccitation.lastpage","961"],["dc.bibliographiccitation.volume","13"],["dc.contributor.author","Zeisberg, Elisabeth M."],["dc.contributor.author","Tarnavski, Oleg"],["dc.contributor.author","Zeisberg, Michael"],["dc.contributor.author","Dorfman, Adam L."],["dc.contributor.author","McMullen, Julie R."],["dc.contributor.author","Gustafsson, Erika"],["dc.contributor.author","Chandraker, Anil"],["dc.contributor.author","Yuan, Xueli"],["dc.contributor.author","Pu, William T."],["dc.contributor.author","Roberts, Anita B."],["dc.contributor.author","Neilson, Eric G."],["dc.contributor.author","Sayegh, Mohamed H."],["dc.contributor.author","Izumo, Seigo"],["dc.contributor.author","Kalluri, Raghu"],["dc.date.accessioned","2020-11-24T12:13:25Z"],["dc.date.available","2020-11-24T12:13:25Z"],["dc.date.issued","2007-08"],["dc.description.abstract","Cardiac fibrosis, associated with a decreased extent of microvasculature and with disruption of normal myocardial structures, results from excessive deposition of extracellular matrix, which is mediated by the recruitment of fibroblasts. The source of these fibroblasts is unclear and specific anti-fibrotic therapies are not currently available. Here we show that cardiac fibrosis is associated with the emergence of fibroblasts originating from endothelial cells, suggesting an endothelial-mesenchymal transition (EndMT) similar to events that occur during formation of the atrioventricular cushion in the embryonic heart. Transforming growth factor-beta1 (TGF-beta1) induced endothelial cells to undergo EndMT, whereas bone morphogenic protein 7 (BMP-7) preserved the endothelial phenotype. The systemic administration of recombinant human BMP-7 (rhBMP-7) significantly inhibited EndMT and the progression of cardiac fibrosis in mouse models of pressure overload and chronic allograft rejection. Our findings show that EndMT contributes to the progression of cardiac fibrosis and that rhBMP-7 can be used to inhibit EndMT and to intervene in the progression of chronic heart disease associated with fibrosis."],["dc.identifier.doi","10.1038/nm1613"],["dc.identifier.pmid","17660828"],["dc.identifier.uri","https://resolver.sub.uni-goettingen.de/purl?gro-2/69173"],["dc.language.iso","en"],["dc.relation.issn","1078-8956"],["dc.title","Endothelial-to-mesenchymal transition contributes to cardiac fibrosis"],["dc.type","journal_article"],["dc.type.internalPublication","unknown"],["dc.type.subtype","original_ja"],["dspace.entity.type","Publication"]]

[["dc.bibliographiccitation.artnumber","eaaz2597"],["dc.bibliographiccitation.issue","635"],["dc.bibliographiccitation.journal","Science Signaling"],["dc.bibliographiccitation.volume","13"],["dc.contributor.author","Lovisa, Sara"],["dc.contributor.author","Fletcher-Sananikone, Eliot"],["dc.contributor.author","Sugimoto, Hikaru"],["dc.contributor.author","Hensel, Janine"],["dc.contributor.author","Lahiri, Sharmistha"],["dc.contributor.author","Hertig, Alexandre"],["dc.contributor.author","Taduri, Gangadhar"],["dc.contributor.author","Lawson, Erica"],["dc.contributor.author","Dewar, Rajan"],["dc.contributor.author","Revuelta, Ignacio"],["dc.contributor.author","Kato, Noritoshi"],["dc.contributor.author","Wu, Chang-Jiun"],["dc.contributor.author","Bassett, Roland L."],["dc.contributor.author","Putluri, Nagireddy"],["dc.contributor.author","Zeisberg, Michael"],["dc.contributor.author","Zeisberg, Elisabeth M."],["dc.contributor.author","LeBleu, Valerie S."],["dc.contributor.author","Kalluri, Raghu"],["dc.date.accessioned","2020-11-24T12:14:26Z"],["dc.date.available","2020-11-24T12:14:26Z"],["dc.date.issued","2020-06-09"],["dc.description.abstract","Endothelial-to-mesenchymal transition (EndMT) is a cellular transdifferentiation program in which endothelial cells partially lose their endothelial identity and acquire mesenchymal-like features. Renal capillary endothelial cells can undergo EndMT in association with persistent damage of the renal parenchyma. The functional consequence(s) of EndMT in kidney fibrosis remains unexplored. Here, we studied the effect of Twist or Snail deficiency in endothelial cells on EndMT in kidney fibrosis. Conditional deletion of Twist1 (which encodes Twist) or Snai1 (which encodes Snail) in VE-cadherin+ or Tie1+ endothelial cells inhibited the emergence of EndMT and improved kidney fibrosis in two different kidney injury/fibrosis mouse models. Suppression of EndMT limited peritubular vascular leakage, reduced tissue hypoxia, and preserved tubular epithelial health and function. Hypoxia, which was exacerbated by EndMT, resulted in increased Myc abundance in tubular epithelial cells, enhanced glycolysis, and suppression of fatty acid oxidation. Pharmacological suppression or epithelial-specific genetic ablation of Myc in tubular epithelial cells ameliorated fibrosis and restored renal parenchymal function and metabolic homeostasis. Together, these findings demonstrate a functional role for EndMT in the response to kidney capillary endothelial injury and highlight the contribution of endothelial-epithelial cross-talk in the development of kidney fibrosis with a potential for therapeutic intervention."],["dc.identifier.doi","10.1126/scisignal.aaz2597"],["dc.identifier.pmid","32518142"],["dc.identifier.uri","https://resolver.sub.uni-goettingen.de/purl?gro-2/69184"],["dc.language.iso","en"],["dc.relation.eissn","1937-9145"],["dc.relation.issn","1945-0877"],["dc.title","Endothelial-to-mesenchymal transition compromises vascular integrity to induce Myc-mediated metabolic reprogramming in kidney fibrosis"],["dc.type","journal_article"],["dc.type.internalPublication","yes"],["dc.type.subtype","original_ja"],["dspace.entity.type","Publication"]]