Tiburcy, Malte

[["dc.bibliographiccitation.firstpage","975"],["dc.bibliographiccitation.issue","8"],["dc.bibliographiccitation.journal","Journal of the American College of Cardiology"],["dc.bibliographiccitation.lastpage","991"],["dc.bibliographiccitation.volume","70"],["dc.contributor.author","Borchert, Thomas"],["dc.contributor.author","Hübscher, Daniela"],["dc.contributor.author","Guessoum, Celina I."],["dc.contributor.author","Lam, Tuan-Dinh D."],["dc.contributor.author","Ghadri, Jelena R."],["dc.contributor.author","Schellinger, Isabel N."],["dc.contributor.author","Tiburcy, Malte"],["dc.contributor.author","Liaw, Norman Y."],["dc.contributor.author","Li, Yun"],["dc.contributor.author","Haas, Jan"],["dc.contributor.author","Sossalla, Samuel"],["dc.contributor.author","Huber, Mia A."],["dc.contributor.author","Cyganek, Lukas"],["dc.contributor.author","Jacobshagen, Claudius"],["dc.contributor.author","Dressel, Ralf"],["dc.contributor.author","Raaz, Uwe"],["dc.contributor.author","Nikolaev, Viacheslav O."],["dc.contributor.author","Guan, Kaomei"],["dc.contributor.author","Thiele, Holger"],["dc.contributor.author","Meder, Benjamin"],["dc.contributor.author","Wollnik, Bernd"],["dc.contributor.author","Zimmermann, Wolfram-Hubertus"],["dc.contributor.author","Lüscher, Thomas F."],["dc.contributor.author","Hasenfuss, Gerd"],["dc.contributor.author","Templin, Christian"],["dc.contributor.author","Streckfuss-Bömeke, Katrin"],["dc.date.accessioned","2018-04-23T11:48:11Z"],["dc.date.available","2018-04-23T11:48:11Z"],["dc.date.issued","2017"],["dc.description.abstract","Background Takotsubo syndrome (TTS) is characterized by an acute left ventricular dysfunction and is associated with life-threating complications in the acute phase. The underlying disease mechanism in TTS is still unknown. A genetic basis has been suggested to be involved in the pathogenesis. Objectives The aims of the study were to establish an in vitro induced pluripotent stem cell (iPSC) model of TTS, to test the hypothesis of altered β-adrenergic signaling in TTS iPSC-cardiomyocytes (CMs), and to explore whether genetic susceptibility underlies the pathophysiology of TTS. Methods Somatic cells of patients with TTS and control subjects were reprogrammed to iPSCs and differentiated into CMs. Three-month-old CMs were subjected to catecholamine stimulation to simulate neurohumoral overstimulation. We investigated β-adrenergic signaling and TTS cardiomyocyte function. Results Enhanced β-adrenergic signaling in TTS-iPSC-CMs under catecholamine-induced stress increased expression of the cardiac stress marker NR4A1; cyclic adenosine monophosphate levels; and cyclic adenosine monophosphate–dependent protein kinase A–mediated hyperphosphorylation of RYR2-S2808, PLN-S16, TNI-S23/24, and Cav1.2-S1928, and leads to a reduced calcium time to transient 50% decay. These cellular catecholamine-dependent responses were mainly mediated by β1-adrenoceptor signaling in TTS. Engineered heart muscles from TTS-iPSC-CMs showed an impaired force of contraction and a higher sensitivity to isoprenaline-stimulated inotropy compared with control subjects. In addition, altered electrical activity and increased lipid accumulation were detected in catecholamine-treated TTS-iPSC-CMs, and were confirmed by differentially expressed lipid transporters CD36 and CPT1C. Furthermore, we uncovered genetic variants in different key regulators of cardiac function. Conclusions Enhanced β-adrenergic signaling and higher sensitivity to catecholamine-induced toxicity were identified as mechanisms associated with the TTS phenotype."],["dc.identifier.doi","10.1016/j.jacc.2017.06.061"],["dc.identifier.gro","3142333"],["dc.identifier.pmid","28818208"],["dc.identifier.purl","https://resolver.sub.uni-goettingen.de/purl?gs-1/16489"],["dc.identifier.uri","https://resolver.sub.uni-goettingen.de/purl?gro-2/13468"],["dc.identifier.url","https://sfb1002.med.uni-goettingen.de/production/literature/publications/204"],["dc.language.iso","en"],["dc.notes.intern","lifescience updates Crossref Import"],["dc.notes.intern","Merged from goescholar"],["dc.notes.status","final"],["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 | D02: Neue Mechanismen der genomischen Instabilität bei Herzinsuffizienz"],["dc.relation.issn","0735-1097"],["dc.relation.workinggroup","RG Cyganek (Stem Cell Unit)"],["dc.relation.workinggroup","RG Dressel"],["dc.relation.workinggroup","RG Guan (Application of patient-specific induced pluripotent stem cells in disease modelling)"],["dc.relation.workinggroup","RG Hasenfuß (Transition zur Herzinsuffizienz)"],["dc.relation.workinggroup","RG Nikolaev (Cardiovascular Research Center)"],["dc.relation.workinggroup","RG Sossalla (Kardiovaskuläre experimentelle Elektrophysiologie und Bildgebung)"],["dc.relation.workinggroup","RG Tiburcy (Stem Cell Disease Modeling)"],["dc.relation.workinggroup","RG Wollnik"],["dc.relation.workinggroup","RG Zimmermann (Engineered Human Myocardium)"],["dc.rights","CC BY-NC-ND 4.0"],["dc.rights.uri","https://creativecommons.org/licenses/by-nc-nd/4.0"],["dc.title","Catecholamine-Dependent β-Adrenergic Signaling in a Pluripotent Stem Cell Model of Takotsubo Cardiomyopathy"],["dc.type","journal_article"],["dc.type.internalPublication","unknown"],["dc.type.peerReviewed","no"],["dc.type.subtype","original_ja"],["dc.type.version","published_version"],["dspace.entity.type","Publication"]]

[["dc.bibliographiccitation.firstpage","1"],["dc.bibliographiccitation.journal","Stem Cells International"],["dc.bibliographiccitation.lastpage","14"],["dc.bibliographiccitation.volume","2018"],["dc.contributor.author","Zhao, Zhihan"],["dc.contributor.author","Lan, Huan"],["dc.contributor.author","El-Battrawy, Ibrahim"],["dc.contributor.author","Li, Xin"],["dc.contributor.author","Buljubasic, Fanis"],["dc.contributor.author","Sattler, Katherine"],["dc.contributor.author","Yücel, Gökhan"],["dc.contributor.author","Lang, Siegfried"],["dc.contributor.author","Tiburcy, Malte"],["dc.contributor.author","Zimmermann, Wolfram-Hubertus"],["dc.contributor.author","Cyganek, Lukas"],["dc.contributor.author","Utikal, Jochen"],["dc.contributor.author","Wieland, Thomas"],["dc.contributor.author","Borggrefe, Martin"],["dc.contributor.author","Zhou, Xiao-Bo"],["dc.contributor.author","Akin, Ibrahim"],["dc.date.accessioned","2020-12-10T18:37:41Z"],["dc.date.available","2020-12-10T18:37:41Z"],["dc.date.issued","2018"],["dc.identifier.doi","10.1155/2018/6067096"],["dc.identifier.pmid","29535773"],["dc.identifier.uri","https://resolver.sub.uni-goettingen.de/purl?gro-2/77065"],["dc.identifier.url","https://sfb1002.med.uni-goettingen.de/production/literature/publications/325"],["dc.language.iso","en"],["dc.notes.intern","DOI Import GROB-354"],["dc.title","Ion Channel Expression and Characterization in Human Induced Pluripotent Stem Cell-Derived Cardiomyocytes"],["dc.type","journal_article"],["dc.type.internalPublication","yes"],["dc.type.subtype","original_ja"],["dspace.entity.type","Publication"]]

[["dc.bibliographiccitation.artnumber","e99941"],["dc.bibliographiccitation.firstpage","1"],["dc.bibliographiccitation.issue","12"],["dc.bibliographiccitation.journal","JCI Insight"],["dc.bibliographiccitation.lastpage","17"],["dc.bibliographiccitation.volume","3"],["dc.contributor.author","Cyganek, Lukas"],["dc.contributor.author","Tiburcy, Malte"],["dc.contributor.author","Sekeres, Karolina"],["dc.contributor.author","Gerstenberg, Kathleen"],["dc.contributor.author","Bohnenberger, Hanibal"],["dc.contributor.author","Lenz, Christof"],["dc.contributor.author","Henze, Sarah"],["dc.contributor.author","Stauske, Michael"],["dc.contributor.author","Salinas, Gabriela"],["dc.contributor.author","Zimmermann, Wolfram-Hubertus"],["dc.contributor.author","Hasenfuss, Gerd"],["dc.contributor.author","Guan, Kaomei"],["dc.date.accessioned","2019-02-04T14:06:58Z"],["dc.date.available","2019-02-04T14:06:58Z"],["dc.date.issued","2018"],["dc.identifier.doi","10.1172/jci.insight.99941"],["dc.identifier.pmid","29925689"],["dc.identifier.uri","https://resolver.sub.uni-goettingen.de/purl?gro-2/57518"],["dc.identifier.url","https://sfb1002.med.uni-goettingen.de/production/literature/publications/214"],["dc.language.iso","en"],["dc.notes.status","final"],["dc.relation","SFB 1002: Modulatorische Einheiten bei Herzinsuffizienz"],["dc.relation","SFB 1002 | A04: Patienten-spezifische induzierte pluripotente Stammzellen zur funktionellen Untersuchung von Ryanodinrezeptor-Mutationen"],["dc.relation","SFB 1002 | D01: Erholung aus der Herzinsuffizienz – Einfluss von Fibrose und Transkriptionssignatur"],["dc.relation","SFB 1002 | C04: Fibroblasten-Kardiomyozyten Interaktion im gesunden und erkrankten Herzen: Mechanismen und therapeutische Interventionen bei Kardiofibroblastopathien"],["dc.relation","SFB 1002 | S01: In vivo und in vitro Krankheitsmodelle"],["dc.relation.issn","0021-9738"],["dc.relation.workinggroup","RG Cyganek (Stem Cell Unit)"],["dc.relation.workinggroup","RG Guan (Application of patient-specific induced pluripotent stem cells in disease modelling)"],["dc.relation.workinggroup","RG Hasenfuß (Transition zur Herzinsuffizienz)"],["dc.relation.workinggroup","RG Lenz"],["dc.relation.workinggroup","RG Tiburcy (Stem Cell Disease Modeling)"],["dc.relation.workinggroup","RG Zimmermann (Engineered Human Myocardium)"],["dc.title","Deep phenotyping of human induced pluripotent stem cell–derived atrial and ventricular cardiomyocytes"],["dc.type","journal_article"],["dc.type.internalPublication","unknown"],["dc.type.subtype","original_ja"],["dspace.entity.type","Publication"]]

[["dc.bibliographiccitation.issue","3"],["dc.bibliographiccitation.journal","Basic Research in Cardiology"],["dc.bibliographiccitation.volume","115"],["dc.contributor.author","Khadjeh, Sara"],["dc.contributor.author","Hindmarsh, Vanessa"],["dc.contributor.author","Weber, Frederike"],["dc.contributor.author","Cyganek, Lukas"],["dc.contributor.author","Vidal, Ramon O."],["dc.contributor.author","Torkieh, Setare"],["dc.contributor.author","Streckfuss-Bömeke, Katrin"],["dc.contributor.author","Lbik, Dawid"],["dc.contributor.author","Tiburcy, Malte"],["dc.contributor.author","Mohamed, Belal A."],["dc.contributor.author","Bonn, Stefan"],["dc.contributor.author","Toischer, Karl"],["dc.contributor.author","Hasenfuss, Gerd"],["dc.date.accessioned","2020-12-10T14:10:26Z"],["dc.date.available","2020-12-10T14:10:26Z"],["dc.date.issued","2020"],["dc.description.abstract","Heart failure is a major health problem worldwide with a significant morbidity and mortality rate. Although studied extensively in animal models, data from patients at the compensated disease stage are lacking. We sampled myocardium biopsies from aortic stenosis patients with compensated hypertrophy and moderate heart failure and used transcriptomics to study the transition to failure. Sequencing and comparative analysis of analogous samples of mice with transverse aortic constriction identified 25 candidate genes with similar regulation in response to pressure overload, reflecting highly conserved molecular processes. The gene cysteine-rich secretory protein LCCL domain containing 1 (CRISPLD1) is upregulated in the transition to failure in human and mouse and its function is unknown. Homology to ion channel regulatory toxins suggests a role in Ca2+ cycling. CRISPR/Cas9-mediated loss-of-function leads to dysregulated Ca2+ handling in human-induced pluripotent stem cell-derived cardiomyocytes. The downregulation of prohypertrophic, proapoptotic and Ca2+-signaling pathways upon CRISPLD1-KO and its upregulation in the transition to failure implicates a contribution to adverse remodeling. These findings provide new pathophysiological data on Ca2+ regulation in the transition to failure and novel candidate genes with promising potential for therapeutic interventions."],["dc.identifier.doi","10.1007/s00395-020-0784-4"],["dc.identifier.pmid","32146539"],["dc.identifier.uri","https://resolver.sub.uni-goettingen.de/purl?gro-2/70757"],["dc.identifier.url","https://sfb1002.med.uni-goettingen.de/production/literature/publications/350"],["dc.language.iso","en"],["dc.notes.intern","DOI Import GROB-354"],["dc.relation","SFB 1002: Modulatorische Einheiten bei Herzinsuffizienz"],["dc.relation","SFB 1002 | C04: Fibroblasten-Kardiomyozyten Interaktion im gesunden und erkrankten Herzen: Mechanismen und therapeutische Interventionen bei Kardiofibroblastopathien"],["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.workinggroup","RG Cyganek (Stem Cell Unit)"],["dc.relation.workinggroup","RG Hasenfuß (Transition zur Herzinsuffizienz)"],["dc.relation.workinggroup","RG Tiburcy (Stem Cell Disease Modeling)"],["dc.relation.workinggroup","RG Toischer (Kardiales Remodeling)"],["dc.rights","CC BY 4.0"],["dc.title","CRISPLD1: a novel conserved target in the transition to human heart failure"],["dc.type","journal_article"],["dc.type.internalPublication","yes"],["dc.type.subtype","original_ja"],["dc.type.version","published_version"],["dspace.entity.type","Publication"]]

[["dc.bibliographiccitation.issue","618"],["dc.bibliographiccitation.journal","Science Translational Medicine"],["dc.bibliographiccitation.volume","13"],["dc.contributor.author","Fomin, Andrey"],["dc.contributor.author","Gärtner, Anna"],["dc.contributor.author","Cyganek, Lukas"],["dc.contributor.author","Tiburcy, Malte"],["dc.contributor.author","Tuleta, Izabela"],["dc.contributor.author","Wellers, Luisa"],["dc.contributor.author","Folsche, Lina"],["dc.contributor.author","Hobbach, Anastasia J."],["dc.contributor.author","von Frieling-Salewsky, Marion"],["dc.contributor.author","Unger, Andreas"],["dc.contributor.author","Linke, Wolfgang A."],["dc.date.accessioned","2021-12-01T09:21:16Z"],["dc.date.available","2021-12-01T09:21:16Z"],["dc.date.issued","2021"],["dc.identifier.doi","10.1126/scitranslmed.abd3079"],["dc.identifier.uri","https://resolver.sub.uni-goettingen.de/purl?gro-2/94394"],["dc.identifier.url","https://mbexc.uni-goettingen.de/literature/publications/363"],["dc.identifier.url","https://sfb1002.med.uni-goettingen.de/production/literature/publications/411"],["dc.language.iso","en"],["dc.notes.intern","DOI-Import GROB-478"],["dc.relation","EXC 2067: Multiscale Bioimaging"],["dc.relation","SFB 1002: Modulatorische Einheiten bei Herzinsuffizienz"],["dc.relation.eissn","1946-6242"],["dc.relation.issn","1946-6234"],["dc.relation.workinggroup","RG Hasenfuß"],["dc.relation.workinggroup","RG Zimmermann (Engineered Human Myocardium)"],["dc.relation.workinggroup","RG Cyganek (Stem Cell Unit)"],["dc.relation.workinggroup","RG Linke (Kardiovaskuläre Physiologie)"],["dc.relation.workinggroup","RG Tiburcy (Stem Cell Disease Modeling)"],["dc.title","Truncated titin proteins and titin haploinsufficiency are targets for functional recovery in human cardiomyopathy due to TTN mutations"],["dc.type","journal_article"],["dc.type.internalPublication","yes"],["dc.type.subtype","original_ja"],["dspace.entity.type","Publication"]]

[["dc.bibliographiccitation.firstpage","f46"],["dc.bibliographiccitation.issue","FI1"],["dc.bibliographiccitation.journal","Europace"],["dc.bibliographiccitation.lastpage","f56"],["dc.bibliographiccitation.volume","20"],["dc.contributor.author","El-Battrawy, Ibrahim"],["dc.contributor.author","Zhao, Zhihan"],["dc.contributor.author","Lan, Huan"],["dc.contributor.author","Cyganek, Lukas"],["dc.contributor.author","Tombers, Christoph"],["dc.contributor.author","Li, Xin"],["dc.contributor.author","Buljubasic, Fanis"],["dc.contributor.author","Lang, Siegfried"],["dc.contributor.author","Tiburcy, Malte"],["dc.contributor.author","Zimmermann, Wolfram-Hubertus"],["dc.contributor.author","Utikal, Jochen"],["dc.contributor.author","Wieland, Thomas"],["dc.contributor.author","Borggrefe, Martin"],["dc.contributor.author","Zhou, Xiao-Bo"],["dc.contributor.author","Akin, Ibrahim"],["dc.date.accessioned","2020-12-10T18:19:08Z"],["dc.date.available","2020-12-10T18:19:08Z"],["dc.date.issued","2018"],["dc.identifier.doi","10.1093/europace/euy042"],["dc.identifier.pmid","29566126"],["dc.identifier.uri","https://resolver.sub.uni-goettingen.de/purl?gro-2/75139"],["dc.identifier.url","https://sfb1002.med.uni-goettingen.de/production/literature/publications/271"],["dc.language.iso","en"],["dc.notes.intern","DOI Import GROB-354"],["dc.title","Electrical dysfunctions in human-induced pluripotent stem cell-derived cardiomyocytes from a patient with an arrhythmogenic right ventricular cardiomyopathy"],["dc.type","journal_article"],["dc.type.internalPublication","yes"],["dc.type.subtype","original_ja"],["dspace.entity.type","Publication"]]

[["dc.bibliographiccitation.firstpage","1059"],["dc.bibliographiccitation.issue","11"],["dc.bibliographiccitation.journal","Circulation"],["dc.bibliographiccitation.lastpage","1076"],["dc.bibliographiccitation.volume","142"],["dc.contributor.author","Hanses, Ulrich"],["dc.contributor.author","Kleinsorge, Mandy"],["dc.contributor.author","Roos, Lennart"],["dc.contributor.author","Yigit, Gökhan"],["dc.contributor.author","Li, Yun"],["dc.contributor.author","Barbarics, Boris"],["dc.contributor.author","El-Battrawy, Ibrahim"],["dc.contributor.author","Lan, Huan"],["dc.contributor.author","Tiburcy, Malte"],["dc.contributor.author","Hindmarsh, Robin"],["dc.contributor.author","Lenz, Christof"],["dc.contributor.author","Salinas, Gabriela"],["dc.contributor.author","Diecke, Sebastian"],["dc.contributor.author","Müller, Christian"],["dc.contributor.author","Adham, Ibrahim"],["dc.contributor.author","Altmüller, Janine"],["dc.contributor.author","Nürnberg, Peter"],["dc.contributor.author","Paul, Thomas"],["dc.contributor.author","Zimmermann, Wolfram-Hubertus"],["dc.contributor.author","Hasenfuss, Gerd"],["dc.contributor.author","Wollnik, Bernd"],["dc.contributor.author","Cyganek, Lukas"],["dc.date.accessioned","2021-04-14T08:32:49Z"],["dc.date.available","2021-04-14T08:32:49Z"],["dc.date.issued","2020"],["dc.identifier.doi","10.1161/CIRCULATIONAHA.119.044794"],["dc.identifier.pmid","32623905"],["dc.identifier.uri","https://resolver.sub.uni-goettingen.de/purl?gro-2/84030"],["dc.identifier.url","https://mbexc.uni-goettingen.de/literature/publications/95"],["dc.identifier.url","https://sfb1002.med.uni-goettingen.de/production/literature/publications/361"],["dc.language.iso","en"],["dc.notes.intern","DOI Import GROB-399"],["dc.relation","EXC 2067: Multiscale Bioimaging"],["dc.relation","SFB 1002: Modulatorische Einheiten bei Herzinsuffizienz"],["dc.relation","SFB 1002 | C04: Fibroblasten-Kardiomyozyten Interaktion im gesunden und erkrankten Herzen: Mechanismen und therapeutische Interventionen bei Kardiofibroblastopathien"],["dc.relation","SFB 1002 | D01: Erholung aus der Herzinsuffizienz – Einfluss von Fibrose und Transkriptionssignatur"],["dc.relation","SFB 1002 | D02: Neue Mechanismen der genomischen Instabilität bei Herzinsuffizienz"],["dc.relation","SFB 1002 | S01: In vivo und in vitro Krankheitsmodelle"],["dc.relation.eissn","1524-4539"],["dc.relation.issn","0009-7322"],["dc.relation.workinggroup","RG Hasenfuß"],["dc.relation.workinggroup","RG Wollnik"],["dc.relation.workinggroup","RG Zimmermann (Engineered Human Myocardium)"],["dc.relation.workinggroup","RG Cyganek (Stem Cell Unit)"],["dc.relation.workinggroup","RG Lenz"],["dc.relation.workinggroup","RG Tiburcy (Stem Cell Disease Modeling)"],["dc.relation.workinggroup","RG Wollnik"],["dc.relation.workinggroup","RG Zimmermann (Engineered Human Myocardium)"],["dc.title","Intronic CRISPR Repair in a Preclinical Model of Noonan Syndrome–Associated Cardiomyopathy"],["dc.type","journal_article"],["dc.type.internalPublication","yes"],["dc.type.subtype","original_ja"],["dspace.entity.type","Publication"]]