Zimmermann, Wolfram-Hubertus

[["dc.bibliographiccitation.firstpage","47"],["dc.bibliographiccitation.issue","1"],["dc.bibliographiccitation.journal","Ultrasound in Medicine & Biology"],["dc.bibliographiccitation.lastpage","55"],["dc.bibliographiccitation.volume","34"],["dc.contributor.author","Wasmeier, Gerald H."],["dc.contributor.author","Zimmermann, Wolfram-Hubertus"],["dc.contributor.author","Schineis, Nico"],["dc.contributor.author","Melnychenko, Ivan"],["dc.contributor.author","Voigt, Jens-Uwe"],["dc.contributor.author","Eschenhagen, Thomas"],["dc.contributor.author","Flachskampf, Frank A."],["dc.contributor.author","Daniel, Werner G."],["dc.contributor.author","Nixdorff, Uwe"],["dc.date.accessioned","2017-09-07T11:48:49Z"],["dc.date.available","2017-09-07T11:48:49Z"],["dc.date.issued","2008"],["dc.description.abstract","Real-time myocardial contrast echocardiography (MCE) is a noninvasive perfusion imaging method, whereas technical and resolution problems impair its application in small animals. Hence, we investigated the feasibility of NICE in experimental cardiovascular set-ups involving healthy and infarcted myocardium in rats. Twenty-five male Wistar rats were examined under volatile anesthesia (2.5% isoflurane) with high-resolution conventional 2-D echocardiography (2DE) and real-time MICE (Sonos 7500 with 15MHz-transducer, Philips Medical Systems, Andover, MA, USA) in short-axis view. Contrast agent (SonoVue, Bracco, Milan, Italy) was infused as a bolus into a sublingual vein. Background-subtracted contrast signal intensity (SI) was measured off-line in six end-systolic segments and fitted to an exponential curve (gamma variate). Derived peak SI was subsequently calculated and compared with wall motion and common functional measured quantities (left ventricular end-diastolic diameter [LVEDD], area shortening [AS]). Recordings were performed before and 14 days after left anterior descending (LAD) ligature. Infarction induced anterior wall motion abnormalities (WMA) in all animals (16 akinetic, 9 hypokinetic), increased LVEDD (9.1 +/- 0.6 vs. 7.9 +/- 0.6 mm, p < 0.001), reduced AS (36.1 +/- 10.0 vs. 59.5 +/- 4.1%, p < 0.001) and reduced anterior segmental SI (0.4 +/- 0.4 dB akinetic / 1.7 +/- 1.7 dB hypokinetic vs. 15.8 +/- 10.9 dB preinfarct, p < 0.001 / p < 0.001). Segmental SI in normokinetic segments remained unchanged. Area at risk (perfusion defect) correlated well with WMA (r = 0.838). These data confirmed high-resolution real-time NICE as a rational tool for assessing myocardial perfusion of Wistar rats. It may therefore be a useful diagnostic tool for ill-vivo cardiovascular research in small animals."],["dc.identifier.doi","10.1016/j.ultrasmedbio.2007.06.027"],["dc.identifier.gro","3143391"],["dc.identifier.isi","000252038900007"],["dc.identifier.pmid","17854980"],["dc.identifier.uri","https://resolver.sub.uni-goettingen.de/purl?gro-2/899"],["dc.notes.intern","WoS Import 2017-03-10"],["dc.notes.status","final"],["dc.notes.submitter","PUB_WoS_Import"],["dc.publisher","Elsevier Science Inc"],["dc.relation.issn","0301-5629"],["dc.title","Real-time myocardial contrast echocardiography for assessing perfusion and function in healthy and infarcted Wistar rats"],["dc.type","journal_article"],["dc.type.internalPublication","yes"],["dc.type.peerReviewed","yes"],["dc.type.subtype","original"],["dspace.entity.type","Publication"]]

[["dc.bibliographiccitation.artnumber","cmdc.202100222"],["dc.bibliographiccitation.firstpage","3300"],["dc.bibliographiccitation.issue","21"],["dc.bibliographiccitation.journal","ChemMedChem"],["dc.bibliographiccitation.lastpage","3305"],["dc.bibliographiccitation.volume","16"],["dc.contributor.affiliation","Raad, Farah S.; 1\r\nInstitute of Pharmacology and Toxicology\r\nUniversity Medical Center\r\nGeorg-August-University\r\nGöttingen Germany"],["dc.contributor.affiliation","Khan, Taukeer A.; 2\r\nDZHK (German Center for Cardiovascular Research) – Partner site Göttingen\r\nGöttingen Germany"],["dc.contributor.affiliation","Esser, Tilman U.; 1\r\nInstitute of Pharmacology and Toxicology\r\nUniversity Medical Center\r\nGeorg-August-University\r\nGöttingen Germany"],["dc.contributor.affiliation","Hudson, James E.; 1\r\nInstitute of Pharmacology and Toxicology\r\nUniversity Medical Center\r\nGeorg-August-University\r\nGöttingen Germany"],["dc.contributor.affiliation","Seth, Bhakti Irene; 1\r\nInstitute of Pharmacology and Toxicology\r\nUniversity Medical Center\r\nGeorg-August-University\r\nGöttingen Germany"],["dc.contributor.affiliation","Fujita, Buntaro; 1\r\nInstitute of Pharmacology and Toxicology\r\nUniversity Medical Center\r\nGeorg-August-University\r\nGöttingen Germany"],["dc.contributor.affiliation","Gandamala, Ravi; 3\r\nInstitute of Organic and Biomolecular Chemistry\r\nGeorg-August-University\r\nGöttingen Germany"],["dc.contributor.affiliation","Tietze, Lutz F.; 2\r\nDZHK (German Center for Cardiovascular Research) – Partner site Göttingen\r\nGöttingen Germany"],["dc.contributor.affiliation","Zimmermann, Wolfram-Hubertus; 1\r\nInstitute of Pharmacology and Toxicology\r\nUniversity Medical Center\r\nGeorg-August-University\r\nGöttingen Germany"],["dc.contributor.author","Raad, Farah S."],["dc.contributor.author","Khan, Taukeer A."],["dc.contributor.author","Esser, Tilman U."],["dc.contributor.author","Hudson, James E."],["dc.contributor.author","Seth, Bhakti Irene"],["dc.contributor.author","Fujita, Buntaro"],["dc.contributor.author","Gandamala, Ravi"],["dc.contributor.author","Tietze, Lutz F."],["dc.contributor.author","Zimmermann, Wolfram H."],["dc.date.accessioned","2021-10-01T09:58:46Z"],["dc.date.available","2021-10-01T09:58:46Z"],["dc.date.issued","2021"],["dc.date.updated","2022-03-21T00:45:29Z"],["dc.description.abstract","Abstract Human pluripotent stem cells (hPSCs) hold great promise for applications in cell therapy and drug screening in the cardiovascular field. Bone morphogenetic protein 4 (BMP4) is key for early cardiac mesoderm induction in hPSC and subsequent cardiomyocyte derivation. Small‐molecular BMP4 mimetics may help to standardize cardiomyocyte derivation from hPSCs. Based on observations that chalcones can stimulate BMP4 signaling pathways, we hypothesized their utility in cardiac mesoderm induction. To test this, we set up a two‐tiered screening strategy, (1) for directed differentiation of hPSCs with commercially available chalcones (4’‐hydroxychalcone [4’HC] and Isoliquiritigen) and 24 newly synthesized chalcone derivatives, and (2) a functional screen to assess the propensity of the obtained cardiomyocytes to self‐organize into contractile engineered human myocardium (EHM). We identified 4’HC, 4‐fluoro‐4’‐methoxychalcone, and 4‐fluoro‐4’‐hydroxychalcone as similarly effective in cardiac mesoderm induction, but only 4’HC as an effective replacement for BMP4 in the derivation of contractile EHM‐forming cardiomyocytes."],["dc.description.abstract","Have a little heart: A screen for mesoderm inducing chalcones in human pluripotent stem cell cultures identified 4’‐hydroxychalcone (4’HC) as an effective replacement for bone‐morphogenetic protein 4 (BMP4) in supporting the derivation of engineered heart muscle (EHM)‐formation competent cardiomyocytes. image"],["dc.description.sponsorship","German Center for Cardiovascular Research"],["dc.description.sponsorship","German Federal Ministry for Science and Education"],["dc.description.sponsorship","German Research Foundation http://dx.doi.org/10.13039/501100001659"],["dc.description.sponsorship","Fondation Leducq http://dx.doi.org/10.13039/501100001674"],["dc.identifier.doi","10.1002/cmdc.202100222"],["dc.identifier.pmid","34309224"],["dc.identifier.uri","https://resolver.sub.uni-goettingen.de/purl?gro-2/90137"],["dc.identifier.url","https://mbexc.uni-goettingen.de/literature/publications/432"],["dc.language.iso","en"],["dc.notes.intern","DOI Import GROB-469"],["dc.relation","EXC 2067: Multiscale Bioimaging"],["dc.relation.eissn","1860-7187"],["dc.relation.issn","1860-7179"],["dc.relation.workinggroup","RG Zimmermann (Engineered Human Myocardium)"],["dc.rights","This is an open access article under the terms of the Creative Commons Attribution License, which permits use, distribution and reproduction in any medium, provided the original work is properly cited."],["dc.title","Chalcone‐Supported Cardiac Mesoderm Induction in Human Pluripotent Stem Cells for Heart Muscle Engineering"],["dc.type","journal_article"],["dc.type.internalPublication","yes"],["dc.type.subtype","original_ja"],["dspace.entity.type","Publication"]]

[["dc.bibliographiccitation.firstpage","219"],["dc.bibliographiccitation.lastpage","239"],["dc.contributor.author","Fujita, Buntaro"],["dc.contributor.author","Tiburcy, Malte"],["dc.contributor.author","Ensminger, Stephan"],["dc.contributor.author","Zimmermann, Wolfram-Hubertus"],["dc.contributor.editor","Ieda, Masaki"],["dc.contributor.editor","Zimmermann, Wolfram-Hubertus"],["dc.date.accessioned","2019-02-27T13:40:08Z"],["dc.date.available","2019-02-27T13:40:08Z"],["dc.date.issued","2017"],["dc.description.abstract","Heart muscle restoration with in vitro engineered tissue constructs is an exciting and rapidly advancing field. Feasibility, safety, and efficacy data have been obtained in animal models. First clinical trials are on the way to explore the therapeutic utility of cell-free and non-contractile cell-containing grafts. Engineering of contractile patches according to current good manufacturing practice (cGMP) for bona fide myocardial re-muscularization and scalability to address clinical demands remains challenging. Proof-of-concept for solutions to address obvious technical hurdles exists, and it can be anticipated that the first generation of clinically applicable engineered heart muscle (EHM) grafts will become available in the near future. Foreseeable, but likely manageable risks include arrhythmia induction and teratoma formation. Remaining biomedical challenges pertain to the requirement of immune suppression and the strategic approach to optimize immune suppression without subjecting the target patient population to an unacceptable risk. This chapter summarizes the current state of tissue-engineered heart repair with a special emphasis on knowledge gained from in vitro and in vivo studies as well as issues pertaining to transplant immunology and cGMP process development."],["dc.identifier.doi","10.1007/978-3-319-56106-6_10"],["dc.identifier.uri","https://resolver.sub.uni-goettingen.de/purl?gro-2/57646"],["dc.identifier.url","https://sfb1002.med.uni-goettingen.de/production/literature/publications/185"],["dc.language.iso","en"],["dc.notes.status","final"],["dc.publisher","Springer"],["dc.publisher.place","Cham, Switzerland"],["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.crisseries","Cardiac and Vascular Biology"],["dc.relation.doi","10.1007/978-3-319-56106-6"],["dc.relation.isbn","978-3-319-56104-2"],["dc.relation.isbn","978-3-319-56106-6"],["dc.relation.ispartof","Cardiac Regeneration"],["dc.relation.ispartofseries","Cardiac and Vascular Biology"],["dc.relation.issn","2509-7830"],["dc.relation.issn","2509-7849"],["dc.relation.workinggroup","RG Tiburcy (Stem Cell Disease Modeling)"],["dc.relation.workinggroup","RG Zimmermann (Engineered Human Myocardium)"],["dc.title","State-of-the-Art in Tissue-Engineered Heart Repair"],["dc.type","book_chapter"],["dc.type.internalPublication","unknown"],["dspace.entity.type","Publication"]]

[["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.artnumber","ehy600"],["dc.bibliographiccitation.firstpage","1"],["dc.bibliographiccitation.journal","European Heart Journal"],["dc.bibliographiccitation.lastpage","19"],["dc.contributor.author","Maack, Christoph"],["dc.contributor.author","Eschenhagen, Thomas"],["dc.contributor.author","Hamdani, Nazha"],["dc.contributor.author","Heinzel, Frank R."],["dc.contributor.author","Lyon, Alexander R."],["dc.contributor.author","Manstein, Dietmar J."],["dc.contributor.author","Metzger, Joseph"],["dc.contributor.author","Papp, Zoltán"],["dc.contributor.author","Tocchetti, Carlo G."],["dc.contributor.author","Yilmaz, M. Birhan"],["dc.contributor.author","Anker, Stefan D."],["dc.contributor.author","Balligand, Jean-Luc"],["dc.contributor.author","Bauersachs, Johann"],["dc.contributor.author","Brutsaert, Dirk"],["dc.contributor.author","Carrier, Lucie"],["dc.contributor.author","Chlopicki, Stefan"],["dc.contributor.author","Cleland, John G."],["dc.contributor.author","de Boer, Rudolf A."],["dc.contributor.author","Dietl, Alexander"],["dc.contributor.author","Fischmeister, Rodolphe"],["dc.contributor.author","Harjola, Veli-Pekka"],["dc.contributor.author","Heymans, Stephane"],["dc.contributor.author","Hilfiker-Kleiner, Denise"],["dc.contributor.author","Holzmeister, Johannes"],["dc.contributor.author","de Keulenaer, Gilles"],["dc.contributor.author","Limongelli, Giuseppe"],["dc.contributor.author","Linke, Wolfgang A."],["dc.contributor.author","Lund, Lars H."],["dc.contributor.author","Masip, Josep"],["dc.contributor.author","Metra, Marco"],["dc.contributor.author","Mueller, Christian"],["dc.contributor.author","Pieske, Burkert"],["dc.contributor.author","Ponikowski, Piotr"],["dc.contributor.author","Ristić, Arsen"],["dc.contributor.author","Ruschitzka, Frank"],["dc.contributor.author","Seferović, Petar M."],["dc.contributor.author","Skouri, Hadi"],["dc.contributor.author","Zimmermann, Wolfram H."],["dc.contributor.author","Mebazaa, Alexandre"],["dc.date.accessioned","2019-02-20T13:50:51Z"],["dc.date.available","2019-02-20T13:50:51Z"],["dc.date.issued","2018"],["dc.description.abstract","Acute heart failure (HF) and in particular, cardiogenic shock are associated with high morbidity and mortality. A therapeutic dilemma is that the use of positive inotropic agents, such as catecholamines or phosphodiesterase-inhibitors, is associated with increased mortality. Newer drugs, such as levosimendan or omecamtiv mecarbil, target sarcomeres to improve systolic function putatively without elevating intracellular Ca2+. Although meta-analyses of smaller trials suggested that levosimendan is associated with a better outcome than dobutamine, larger comparative trials failed to confirm this observation. For omecamtiv mecarbil, Phase II clinical trials suggest a favourable haemodynamic profile in patients with acute and chronic HF, and a Phase III morbidity/mortality trial in patients with chronic HF has recently begun. Here, we review the pathophysiological basis of systolic dysfunction in patients with HF and the mechanisms through which different inotropic agents improve cardiac function. Since adenosine triphosphate and reactive oxygen species production in mitochondria are intimately linked to the processes of excitation–contraction coupling, we also discuss the impact of inotropic agents on mitochondrial bioenergetics and redox regulation. Therefore, this position paper should help identify novel targets for treatments that could not only safely improve systolic and diastolic function acutely, but potentially also myocardial structure and function over a longer-term."],["dc.identifier.doi","10.1093/eurheartj/ehy600"],["dc.identifier.pmid","30295807"],["dc.identifier.uri","https://resolver.sub.uni-goettingen.de/purl?gro-2/57605"],["dc.identifier.url","https://sfb1002.med.uni-goettingen.de/production/literature/publications/235"],["dc.language.iso","en"],["dc.notes.status","fcwi"],["dc.relation","SFB 1002: Modulatorische Einheiten bei Herzinsuffizienz"],["dc.relation","SFB 1002 | C01: Epigenetische Kontrolle der Herzfibrose"],["dc.relation","SFB 1002 | C04: Fibroblasten-Kardiomyozyten Interaktion im gesunden und erkrankten Herzen: Mechanismen und therapeutische Interventionen bei Kardiofibroblastopathien"],["dc.relation.workinggroup","RG Linke (Kardiovaskuläre Physiologie)"],["dc.relation.workinggroup","RG Zimmermann (Engineered Human Myocardium)"],["dc.title","Treatments targeting inotropy"],["dc.type","journal_article"],["dc.type.internalPublication","unknown"],["dc.type.subtype","original_ja"],["dspace.entity.type","Publication"]]

[["dc.bibliographiccitation.journal","Journal of Molecular and Cellular Cardiology"],["dc.contributor.author","Jebran, Ahmad-Fawad"],["dc.contributor.author","Tiburcy, Malte"],["dc.contributor.author","Biermann, Daniel"],["dc.contributor.author","Balfanz, Paul"],["dc.contributor.author","Didié, Michael"],["dc.contributor.author","Karikkineth, Bijoy Chandapillai"],["dc.contributor.author","Schöndube, Friedrich"],["dc.contributor.author","Kutschka, Ingo"],["dc.contributor.author","Zimmermann, Wolfram-Hubertus"],["dc.date.accessioned","2022-04-14T07:06:38Z"],["dc.date.available","2022-04-14T07:06:38Z"],["dc.date.issued","2022-04-04"],["dc.description.abstract","Engineered heart muscle (EHM) can be implanted epicardially to remuscularize the failing heart. In case of a severely scarred ventricle, excision of scar followed by transmural heart wall replacement may be a more desirable application. Accordingly, we tested the hypothesis that allograft (rat) and xenograft (human) EHM can also be administered as transmural heart wall replacement in a heterotopic, volume-loaded heart transplantation model. We first established a novel rat model model to test surgical transmural left heart wall repair. Subsequently and in continuation of our previous allograft studies, we tested outcome after implantation of contractile engineered heart muscle (EHM) and non-contractile engineered connective tissue (ECT) as well as engineered mesenchymal tissue (EMT) allografts as transmural heart wall replacement. Finally, proof-of-concept for the application of human EHM was obtained in an athymic nude rat model. Only in case of EHM implantation, remuscularization of the surgically created transmural defect was observed with palpable graft vascularization. Taken together, feasibility of transmural heart repair using bioengineered myocardial grafts could be demonstrated in a novel rat model of heterotopic heart transplantation."],["dc.identifier.doi","10.1016/j.yjmcc.2022.03.013"],["dc.identifier.pmid","35390437"],["dc.identifier.uri","https://resolver.sub.uni-goettingen.de/purl?gro-2/106523"],["dc.identifier.url","https://mbexc.uni-goettingen.de/literature/publications/473"],["dc.identifier.url","https://sfb1002.med.uni-goettingen.de/production/literature/publications/427"],["dc.language.iso","en"],["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.eissn","1095-8584"],["dc.relation.issn","0022-2828"],["dc.relation.workinggroup","RG Zimmermann (Engineered Human Myocardium)"],["dc.title","Transmural myocardial repair with engineered heart muscle in a rat model of heterotopic heart transplantation - A proof-of-concept study"],["dc.type","journal_article"],["dc.type.internalPublication","yes"],["dc.type.subtype","original_ja"],["dspace.entity.type","Publication"]]

[["dc.bibliographiccitation.firstpage","51"],["dc.bibliographiccitation.journal","Progress in Biophysics and Molecular Biology"],["dc.bibliographiccitation.lastpage","60"],["dc.bibliographiccitation.volume","144"],["dc.contributor.author","Schlick, Susanne F."],["dc.contributor.author","Spreckelsen, Florian"],["dc.contributor.author","Tiburcy, Malte"],["dc.contributor.author","Iyer, Lavanya M."],["dc.contributor.author","Meyer, Tim"],["dc.contributor.author","Zelarayan, Laura C."],["dc.contributor.author","Luther, Stefan"],["dc.contributor.author","Parlitz, Ulrich"],["dc.contributor.author","Zimmermann, Wolfram-Hubertus"],["dc.contributor.author","Rehfeldt, Florian"],["dc.date.accessioned","2020-12-10T15:20:42Z"],["dc.date.available","2020-12-10T15:20:42Z"],["dc.date.issued","2019"],["dc.description.abstract","Cardiomyocyte and stroma cell cross-talk is essential for the formation of collagen-based engineered heart muscle, including engineered human myocardium (EHM). Fibroblasts are a main component of the myocardial stroma. We hypothesize that fibroblasts, by compacting the surrounding collagen network, support the self-organization of cardiomyocytes into a functional syncytium. With a focus on early self-organization processes in EHM, we studied the molecular and biophysical adaptations mediated by defined populations of fibroblasts and embryonic stem cell-derived cardiomyocytes in a collagen type I hydrogel. After a short phase of cell-independent collagen gelation (30 min), tissue compaction was progressively mediated by fibroblasts. Fibroblast-mediated tissue stiffening was attenuated in the presence of cardiomyocytes allowing for the assembly of stably contracting, force-generating EHM within 4 weeks. Comparative RNA-sequencing data corroborated that fibroblasts are particularly sensitive to the tissue compaction process, resulting in the fast activation of transcription profiles, supporting heart muscle development and extracellular matrix synthesis. Large amplitude oscillatory shear (LAOS) measurements revealed nonlinear strain stiffening at physiological strain amplitudes (>2%), which was reduced in the presence of cells. The nonlinear stress-strain response could be characterized by a mathematical model. Collectively, our study defines the interplay between fibroblasts and cardiomyocytes during human heart muscle self-organization in vitro and underscores the relevance of fibroblasts in the biological engineering of a cardiomyogenesis-supporting viscoelastic stroma. We anticipate that the established mathematical model will facilitate future attempts to optimize EHM for in vitro (disease modelling) and in vivo applications (heart repair)."],["dc.identifier.doi","10.1016/j.pbiomolbio.2018.11.011"],["dc.identifier.pmid","30553553"],["dc.identifier.uri","https://resolver.sub.uni-goettingen.de/purl?gro-2/72769"],["dc.identifier.url","https://sfb1002.med.uni-goettingen.de/production/literature/publications/248"],["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 | S01: In vivo und in vitro Krankheitsmodelle"],["dc.relation.workinggroup","RG Luther (Biomedical Physics)"],["dc.relation.workinggroup","RG Tiburcy (Stem Cell Disease Modeling)"],["dc.relation.workinggroup","RG Zelarayán-Behrend (Developmental Pharmacology)"],["dc.relation.workinggroup","RG Zimmermann (Engineered Human Myocardium)"],["dc.rights","CC BY 4.0"],["dc.title","Agonistic and antagonistic roles of fibroblasts and cardiomyocytes on viscoelastic stiffening of engineered human myocardium"],["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","1"],["dc.bibliographiccitation.journal","Progress in Biophysics and Molecular Biology"],["dc.bibliographiccitation.lastpage","2"],["dc.bibliographiccitation.volume","144"],["dc.contributor.author","Tarantola, Marco"],["dc.contributor.author","Meyer, Tim"],["dc.contributor.author","Schmidt, Christoph F."],["dc.contributor.author","Zimmermann, Wolfram-Hubertus"],["dc.date.accessioned","2020-12-10T15:20:42Z"],["dc.date.available","2020-12-10T15:20:42Z"],["dc.date.issued","2019"],["dc.identifier.doi","10.1016/j.pbiomolbio.2019.03.009"],["dc.identifier.issn","0079-6107"],["dc.identifier.uri","https://resolver.sub.uni-goettingen.de/purl?gro-2/72770"],["dc.language.iso","en"],["dc.notes.intern","DOI Import GROB-354"],["dc.title","Physics meets medicine - At the heart of active matter"],["dc.type","journal_article"],["dc.type.internalPublication","yes"],["dspace.entity.type","Publication"]]

[["dc.bibliographiccitation.journal","Acta Physiologica"],["dc.bibliographiccitation.volume","216"],["dc.contributor.author","Jatho, Aline"],["dc.contributor.author","Hartmann, S."],["dc.contributor.author","Kittana, Naim"],["dc.contributor.author","Muegge, F."],["dc.contributor.author","Wuertz, Christina"],["dc.contributor.author","Tiburcy, Malte"],["dc.contributor.author","Zimmermann, Wolfram-Hubertus"],["dc.contributor.author","Katschinski, Doerthe Magdalena"],["dc.contributor.author","Lutz, S."],["dc.date.accessioned","2018-11-07T10:17:27Z"],["dc.date.available","2018-11-07T10:17:27Z"],["dc.date.issued","2016"],["dc.identifier.isi","000372285400124"],["dc.identifier.uri","https://resolver.sub.uni-goettingen.de/purl?gro-2/41230"],["dc.notes.status","zu prüfen"],["dc.notes.submitter","Najko"],["dc.publisher","Wiley-blackwell"],["dc.publisher.place","Hoboken"],["dc.relation.issn","1748-1716"],["dc.relation.issn","1748-1708"],["dc.title","RhoA ambivalently controls prominent myofibroblast characteristics by involving distinct signaling routes"],["dc.type","conference_abstract"],["dc.type.internalPublication","yes"],["dc.type.peerReviewed","yes"],["dc.type.status","published"],["dspace.entity.type","Publication"]]

[["dc.bibliographiccitation.artnumber","78"],["dc.bibliographiccitation.issue","9"],["dc.bibliographiccitation.journal","Current Cardiology Reports"],["dc.bibliographiccitation.volume","19"],["dc.contributor.author","Fujita, Buntaro"],["dc.contributor.author","Zimmermann, Wolfram-Hubertus"],["dc.date.accessioned","2018-04-23T11:49:18Z"],["dc.date.available","2018-04-23T11:49:18Z"],["dc.date.issued","2017"],["dc.description.abstract","Purpose of Review This review provides an overview of the current state of tissue-engineered heart repair with a special focus on the anticipated modes of action of tissue-engineered therapy candidates and particular implications as to transplant immunology. Recent Findings Myocardial tissue engineering technologies have made tremendous advances in recent years. Numerous different strategies are under investigation and have reached different stages on their way to clinical translation. Studies in animal models demonstrated that heart repair requires either remuscularization by delivery of bona fide cardiomyocytes or paracrine support for the activation of endogenous repair mechanisms. Tissue engineering approaches result in enhanced cardiomyocyte retention and sustained remuscularization, but may also be explored for targeted paracrine or mechanical support. Some of the more advanced tissue engineering approaches are already tested clinically; others are at late stages of pre-clinical development. Process optimization towards cGMP compatibility and clinical scalability of contractile engineered human myocardium is an essential step towards clinical translation. Long-term allograft retention can be achieved under immune suppression. HLA matching may be an option to enhance graft retention and reduce the need for comprehensive immune suppression. Summary Tissue-engineered heart repair is entering the clinical stage of the translational pipeline. Like in any effective therapy, side effects must be anticipated and carefully controlled. Allograft implantation under immune suppression is the most likely clinical scenario. Strategies to overcome transplant rejection are evolving and may further boost the clinical acceptance of tissue-engineered heart repair."],["dc.identifier.doi","10.1007/s11886-017-0892-4"],["dc.identifier.gro","3142520"],["dc.identifier.uri","https://resolver.sub.uni-goettingen.de/purl?gro-2/13675"],["dc.identifier.url","https://sfb1002.med.uni-goettingen.de/production/literature/publications/174"],["dc.language.iso","en"],["dc.notes.intern","lifescience updates Crossref Import"],["dc.notes.status","final"],["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 | S01: In vivo und in vitro Krankheitsmodelle"],["dc.relation.issn","1523-3782"],["dc.relation.workinggroup","RG Zimmermann (Engineered Human Myocardium)"],["dc.title","Myocardial Tissue Engineering for Regenerative Applications"],["dc.type","journal_article"],["dc.type.internalPublication","unknown"],["dc.type.peerReviewed","no"],["dc.type.subtype","overview_ja"],["dspace.entity.type","Publication"]]