Eschenhagen, Thomas

[["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","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.firstpage","909"],["dc.bibliographiccitation.issue","4"],["dc.bibliographiccitation.journal","Hepatology"],["dc.bibliographiccitation.lastpage","918"],["dc.bibliographiccitation.volume","38"],["dc.contributor.author","Sass, Gabriele"],["dc.contributor.author","Soares, Miguel Che Parreira"],["dc.contributor.author","Yamashita, Kenichiro"],["dc.contributor.author","Seyfried, Stefan"],["dc.contributor.author","Zimmermann, Wolfram-Hubertus"],["dc.contributor.author","Eschenhagen, Thomas"],["dc.contributor.author","Kaczmarek, Elzbieta"],["dc.contributor.author","Ritter, Thomas"],["dc.contributor.author","Volk, Hans-Dieter"],["dc.contributor.author","Tiegs, Gisa"],["dc.date.accessioned","2017-09-07T11:54:28Z"],["dc.date.available","2017-09-07T11:54:28Z"],["dc.date.issued","2003"],["dc.description.abstract","Heme oxygenase‐1 (HO‐1), a stress‐responsive enzyme that catabolizes heme into carbon monoxide (CO), biliverdin, and iron, has previously been shown to protect grafts from ischemia/reperfusion injury and rejection. Here we investigated the protective potential of HO‐1 in 5 models of immune‐mediated liver injury. We found that up‐regulation of endogenous HO‐1 by cobalt‐protoporphyrin‐IX (CoPP) protected mice from apoptotic liver damage induced by anti‐CD95 antibody (Ab) or D‐galactosamine in combination with either anti‐CD3 Ab, lipopolysaccharide (LPS), or tumor necrosis factor α (TNF‐α). HO‐1 induction prevented apoptotic liver injury, measured by inhibition of caspase 3 activation, although it did not protect mice from caspase‐3—independent necrotic liver damage caused by concanavalin A (Con A) administration. In addition, overexpression of HO‐1 by adenoviral gene transfer resulted in protection from apoptotic liver injury, whereas inhibition of HO‐1 enzymatic activity by tin‐protoporphyrin‐IX (SnPP) abrogated the protective effect. HO‐1—mediated protection seems to target parenchymal liver cells directly because CoPP treatment protected isolated primary hepatocytes from anti‐CD95—induced apoptosis in vitro. Furthermore, depletion of Kupffer cells (KCs) did not interfere with the protective effect in vivo. Exogenous CO administration or treatment with the CO‐releasing agent methylene chloride mimicked the protective effect of HO‐1, whereas treatment with exogenous biliverdin or overexpression of ferritin by recombinant adenoviral gene transfer did not. In conclusion, HO‐1 is a potent protective factor for cytokine‐ and CD95‐mediated apoptotic liver damage. Induction of HO‐1 might be of a therapeutic modality for inflammatory liver diseases."],["dc.identifier.doi","10.1002/hep.1840380417"],["dc.identifier.gro","3145182"],["dc.identifier.pii","S0270-9139(03)00677-3"],["dc.identifier.uri","https://resolver.sub.uni-goettingen.de/purl?gro-2/2889"],["dc.language.iso","en"],["dc.notes.intern","Crossref Import"],["dc.notes.status","final"],["dc.relation.issn","0270-9139"],["dc.title","Heme oxygenase-1 and its reaction product, carbon monoxide, prevent inflammation-related apoptotic liver damage in mice"],["dc.type","journal_article"],["dc.type.internalPublication","no"],["dc.type.peerReviewed","no"],["dspace.entity.type","Publication"]]

[["dc.bibliographiccitation.firstpage","31"],["dc.bibliographiccitation.journal","Journal of Molecular and Cellular Cardiology"],["dc.bibliographiccitation.lastpage","43"],["dc.bibliographiccitation.volume","127"],["dc.contributor.author","Morhenn, Karoline"],["dc.contributor.author","Quentin, Thomas"],["dc.contributor.author","Wichmann, Helen"],["dc.contributor.author","Steinmetz, Michael"],["dc.contributor.author","Prondzynski, Maksymilian"],["dc.contributor.author","Söhren, Klaus-Dieter"],["dc.contributor.author","Christ, Torsten"],["dc.contributor.author","Geertz, Birgit"],["dc.contributor.author","Schröder, Sabine"],["dc.contributor.author","Schöndube, Friedrich A."],["dc.contributor.author","Hasenfuss, Gerd"],["dc.contributor.author","Schlossarek, Saskia"],["dc.contributor.author","Zimmermann, Wolfram H."],["dc.contributor.author","Carrier, Lucie"],["dc.contributor.author","Eschenhagen, Thomas"],["dc.contributor.author","Cardinaux, Jean-René"],["dc.contributor.author","Lutz, Susanne"],["dc.contributor.author","Oetjen, Elke"],["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.2018.12.001"],["dc.identifier.issn","0022-2828"],["dc.identifier.uri","https://resolver.sub.uni-goettingen.de/purl?gro-2/73167"],["dc.language.iso","en"],["dc.notes.intern","DOI Import GROB-354"],["dc.title","Mechanistic role of the CREB-regulated transcription coactivator 1 in cardiac hypertrophy"],["dc.type","journal_article"],["dc.type.internalPublication","yes"],["dspace.entity.type","Publication"]]

[["dc.bibliographiccitation.journal","Naunyn-Schmiedeberg s Archives of Pharmacology"],["dc.bibliographiccitation.volume","383"],["dc.contributor.author","Neuber, C."],["dc.contributor.author","Eder, Alexandra"],["dc.contributor.author","Hansen, A."],["dc.contributor.author","Mueller, Oliver J."],["dc.contributor.author","Sietmann, A."],["dc.contributor.author","Ruehle, Frank"],["dc.contributor.author","Stoll, Monika"],["dc.contributor.author","Eschenhagen, Thomas"],["dc.contributor.author","El-Armouche, Ali"],["dc.date.accessioned","2018-11-07T08:58:33Z"],["dc.date.available","2018-11-07T08:58:33Z"],["dc.date.issued","2011"],["dc.format.extent","66"],["dc.identifier.isi","000288573100329"],["dc.identifier.uri","https://resolver.sub.uni-goettingen.de/purl?gro-2/23669"],["dc.notes.status","zu prüfen"],["dc.notes.submitter","Najko"],["dc.publisher","Springer"],["dc.publisher.place","New york"],["dc.relation.conference","77th Annual Meeting on German-Society-for-Experimental-and-Clinical-Pharmacology-and-Toxicology"],["dc.relation.eventlocation","Frankfurt, GERMANY"],["dc.relation.issn","0028-1298"],["dc.title","AAV-mediated knockdown of the beta(1)-adrenoceptor in reconstituted heart tissue"],["dc.type","conference_abstract"],["dc.type.internalPublication","yes"],["dc.type.peerReviewed","yes"],["dc.type.status","published"],["dspace.entity.type","Publication"]]

[["dc.bibliographiccitation.journal","Cardiovascular Research"],["dc.bibliographiccitation.volume","103"],["dc.contributor.author","Neuber, C."],["dc.contributor.author","Uebeler, June"],["dc.contributor.author","Schulze, T."],["dc.contributor.author","Sotoud, Hannieh"],["dc.contributor.author","El-Armouche, Ali"],["dc.contributor.author","Eschenhagen, Thomas"],["dc.date.accessioned","2018-11-07T09:37:38Z"],["dc.date.available","2018-11-07T09:37:38Z"],["dc.date.issued","2014"],["dc.identifier.doi","10.1093/cvr/cvu091.52"],["dc.identifier.isi","000343730100283"],["dc.identifier.uri","https://resolver.sub.uni-goettingen.de/purl?gro-2/32884"],["dc.notes.status","zu prüfen"],["dc.notes.submitter","Najko"],["dc.publisher","Oxford Univ Press"],["dc.publisher.place","Oxford"],["dc.relation.conference","3rd Congress of the ESC-Council-on-Basic-Cardiovascular-Science on Frontiers in Cardio Vascular Biology"],["dc.relation.eventlocation","Barcelona, SPAIN"],["dc.relation.issn","1755-3245"],["dc.relation.issn","0008-6363"],["dc.title","Guanabenz interferes with ER stress and exerts protective effects in cardiac myocytes"],["dc.type","conference_abstract"],["dc.type.internalPublication","yes"],["dc.type.peerReviewed","yes"],["dc.type.status","published"],["dspace.entity.type","Publication"]]

[["dc.bibliographiccitation.firstpage","452"],["dc.bibliographiccitation.issue","4"],["dc.bibliographiccitation.journal","Nature Medicine"],["dc.bibliographiccitation.lastpage","458"],["dc.bibliographiccitation.volume","12"],["dc.contributor.author","Zimmermann, Wolfram-Hubertus"],["dc.contributor.author","Melnychenko, Ivan"],["dc.contributor.author","Wasmeier, Gerald H."],["dc.contributor.author","Didie, Michael"],["dc.contributor.author","Naito, Hiroshi"],["dc.contributor.author","Nixdorff, U"],["dc.contributor.author","Hess, Andreas"],["dc.contributor.author","Budinsky, L."],["dc.contributor.author","Brune, K"],["dc.contributor.author","Michaelis, B."],["dc.contributor.author","Dhein, S."],["dc.contributor.author","Schwoerer, Alexander Peter"],["dc.contributor.author","Ehmke, Heimo"],["dc.contributor.author","Eschenhagen, Thomas"],["dc.date.accessioned","2017-09-07T11:53:08Z"],["dc.date.available","2017-09-07T11:53:08Z"],["dc.date.issued","2006"],["dc.description.abstract","The concept of regenerating diseased myocardium by implantation of tissue-engineered heart muscle is intriguing, but convincing evidence is lacking that heart tissues can be generated at a size and with contractile properties that would lend considerable support to failing hearts. Here we created large (thickness/ diameter, 1-4 mm/15 mm), force-generating engineered heart tissue from neonatal rat heart cells. Engineered heart tissue formed thick cardiac muscle layers when implanted on myocardial infarcts in immune-suppressed rats. When evaluated 28 d later, engineered heart tissue showed undelayed electrical coupling to the native myocardium without evidence of arrhythmia induction. Moreover, engineered heart tissue prevented further dilation, induced systolic wall thickening of infarcted myocardial segments and improved fractional area shortening of infarcted hearts compared to controls (sham operation and noncontractile constructs). Thus, our study provides evidence that large contractile cardiac tissue grafts can be constructed in vitro, can survive after implantation and can support contractile function of infarcted hearts."],["dc.identifier.doi","10.1038/nm1394"],["dc.identifier.gro","3143714"],["dc.identifier.isi","000236581300035"],["dc.identifier.pmid","16582915"],["dc.identifier.uri","https://resolver.sub.uni-goettingen.de/purl?gro-2/1259"],["dc.notes.intern","WoS Import 2017-03-10"],["dc.notes.status","final"],["dc.notes.submitter","PUB_WoS_Import"],["dc.publisher","Nature Publishing Group"],["dc.relation.issn","1078-8956"],["dc.title","Engineered heart tissue grafts improve systolic and diastolic function in infarcted rat hearts"],["dc.type","journal_article"],["dc.type.internalPublication","yes"],["dc.type.peerReviewed","yes"],["dc.type.subtype","original"],["dspace.entity.type","Publication"]]

[["dc.bibliographiccitation.firstpage","90"],["dc.bibliographiccitation.issue","1"],["dc.bibliographiccitation.journal","Cardiovascular Research"],["dc.bibliographiccitation.lastpage","102"],["dc.bibliographiccitation.volume","109"],["dc.contributor.author","Flenner, Frederik"],["dc.contributor.author","Friedrich, Felix W."],["dc.contributor.author","Ungeheuer, Nele"],["dc.contributor.author","Christ, Torsten"],["dc.contributor.author","Geertz, Birgit"],["dc.contributor.author","Reischmann, Silke"],["dc.contributor.author","Wagner, Stefan"],["dc.contributor.author","Stathopoulou, Konstantina"],["dc.contributor.author","Soehren, Klaus-Dieter"],["dc.contributor.author","Weinberger, Florian"],["dc.contributor.author","Schwedhelm, Edzard"],["dc.contributor.author","Cuello, Friederike"],["dc.contributor.author","Maier, Lars. S."],["dc.contributor.author","Eschenhagen, Thomas"],["dc.contributor.author","Carrier, Lucie"],["dc.date.accessioned","2018-11-07T10:21:19Z"],["dc.date.available","2018-11-07T10:21:19Z"],["dc.date.issued","2016"],["dc.description.abstract","Aims Hypertrophic cardiomyopathy (HCM) is often accompanied by increased myofilament Ca2+ sensitivity and diastolic dysfunction. Recent findings indicate increased late Na+ current density in human HCM cardiomyocytes. Since ranolazine has the potential to decrease myofilament Ca2+ sensitivity and late Na+ current, we investigated its effects in an Mybpc3-targeted knock-in (KI) mouse model of HCM. Methods and results Unloaded sarcomere shortening and Ca2+ transients were measured in KI and wild-type (WT) cardiomyocytes. Measurements were performed at baseline (1 Hz) and under increased workload (30 nM isoprenaline (ISO), 5 Hz) in the absence or presence of 10 mu M ranolazine. KI myocytes showed shorter diastolic sarcomere length at baseline, stronger inotropic response to ISO, and drastic drop of diastolic sarcomere length under increased workload. Ranolazine attenuated ISO responses in WT and KI cells and prevented workload-induced diastolic failure in KI. Late Na+ current density was diminished and insensitive to ranolazine in KI cardiomyocytes. Ca2+ sensitivity of skinned KI trabeculae was slightly decreased by ranolazine. Phosphorylation analysis of cAMP-dependent protein kinase A-target proteins and ISO concentration-response measurements on muscle strips indicated antagonism at beta-adrenoceptors with 10 mu M ranolazine shifting the ISO response by 0.6 log units. Six-month treatment with ranolazine (plasma level > 20 mu M) demonstrated a beta-blocking effect, but did not reverse cardiac hypertrophy or dysfunction in KI mice. Conclusion Ranolazine improved tolerance to high workload in mouse HCM cardiomyocytes, not by blocking late Na+ current, but by antagonizing beta-adrenergic stimulation and slightly desensitizing myofilaments to Ca2+. This effect did not translate in therapeutic efficacy in vivo."],["dc.identifier.doi","10.1093/cvr/cvv247"],["dc.identifier.isi","000368414600011"],["dc.identifier.pmid","26531128"],["dc.identifier.uri","https://resolver.sub.uni-goettingen.de/purl?gro-2/42059"],["dc.notes.status","zu prüfen"],["dc.notes.submitter","Najko"],["dc.publisher","Oxford Univ Press"],["dc.relation.issn","1755-3245"],["dc.relation.issn","0008-6363"],["dc.title","Ranolazine antagonizes catecholamine-induced dysfunction in isolated cardiomyocytes, but lacks long-term therapeutic effects in vivo in a mouse model of hypertrophic cardiomyopathy"],["dc.type","journal_article"],["dc.type.internalPublication","yes"],["dc.type.peerReviewed","yes"],["dc.type.status","published"],["dspace.entity.type","Publication"]]

[["dc.bibliographiccitation.firstpage","435"],["dc.bibliographiccitation.issue","4"],["dc.bibliographiccitation.journal","Future Cardiology"],["dc.bibliographiccitation.lastpage","445"],["dc.bibliographiccitation.volume","3"],["dc.contributor.author","Zimmermann, Wolfram-Hubertus"],["dc.contributor.author","Tiburcy, Malte"],["dc.contributor.author","Eschenhagen, Thomas"],["dc.date.accessioned","2017-09-07T11:54:28Z"],["dc.date.available","2017-09-07T11:54:28Z"],["dc.date.issued","2011"],["dc.description.abstract","Engineered myocardium may be used to repair myocardial defects. Although not clinically applicable yet, initial studies in rodents have demonstrated the feasibility of tissue engineering based myocardial repair in vivo. In order for restorative treatment to evolve into a functional treatment modality, tissue engineers have to generate human myocardium of sufficient size and with relevant contractile function to replace/repair myocardial defects. This requires the identification of a scalable and ideally autologous cardiomyocyte source as well as the development of strategies to overcome size limitations. We will further address pivotal issues pertaining to the allocation of suitable human cells for myocardial tissue engineering and discuss the translation of present myocardial tissue engineering concepts into preclinical, as well as clinical, trials."],["dc.identifier.doi","10.2217/14796678.3.4.435"],["dc.identifier.gro","3145184"],["dc.identifier.uri","https://resolver.sub.uni-goettingen.de/purl?gro-2/2892"],["dc.language.iso","en"],["dc.notes.intern","Crossref Import"],["dc.notes.status","final"],["dc.relation.issn","1479-6678"],["dc.title","Cardiac tissue engineering: a clinical perspective"],["dc.type","journal_article"],["dc.type.internalPublication","unknown"],["dc.type.peerReviewed","no"],["dspace.entity.type","Publication"]]

[["dc.bibliographiccitation.firstpage","S247"],["dc.bibliographiccitation.issue","11"],["dc.bibliographiccitation.lastpage","S254"],["dc.bibliographiccitation.volume","120"],["dc.contributor.author","Deuse, Tobias"],["dc.contributor.author","Peter, Christoph"],["dc.contributor.author","Fedak, Paul W. M."],["dc.contributor.author","Doyle, Tim"],["dc.contributor.author","Reichenspurner, Hermann"],["dc.contributor.author","Zimmermann, Wolfram-Hubertus"],["dc.contributor.author","Eschenhagen, Thomas"],["dc.contributor.author","Stein, William"],["dc.contributor.author","Wu, Joseph C."],["dc.contributor.author","Robbins, Robert C."],["dc.contributor.author","Schrepfer, Sonja"],["dc.date.accessioned","2017-09-07T11:46:49Z"],["dc.date.available","2017-09-07T11:46:49Z"],["dc.date.issued","2009"],["dc.description.abstract","Background-Mesenchymal stem cell (MSC)-based regenerative strategies were investigated to treat acute myocardial infarction and improve left ventricular function. Methods and Results-Murine AMI was induced by coronary ligation with subsequent injection of MSCs, hepatocyte growth factor (HGF), vascular endothelial growth factor (VEGF), or MSCs +HGF/VEGF into the border zone. Left ventricular ejection fraction was calculated using micro-computed tomography imaging after 6 months. HGF and VEGF protein injection (with or without concomitant MSC injection) significantly and similarly improved the left ventricular ejection fraction and reduced scar size compared with the MSC group, suggesting that myocardial recovery was due to the cytokines rather than myocardial regeneration. To provide sustained paracrine effects, HGF or VEGF overexpressing MSCs were generated (MSC-HGF, MSC-VEGF). MSC-HGF and MSC-VEGF showed significantly increased in vitro proliferation and increased in vivo proliferation within the border zone. Cytokine production correlated with MSC survival. MSC-HGF-and MSC-VEGF-treated animals showed smaller scar sizes, increased peri-infarct vessel densities, and better preserved left ventricular function when compared with MSCs transfected with empty vector. Murine cardiomyocytes were exposed to hypoxic in vitro conditions. The LDH release was reduced, fewer cardiomyocytes were apoptotic, and Akt activity was increased if cardiomyocytes were maintained in conditioned medium obtained from MSC-HGF or MSC-VEGF cultures. Conclusions-This study showed that (1) elevating the tissue levels of HGF and VEGF after acute myocardial infarction seems to be a promising reparative therapeutic approach, (2) HGF and VEGF are cardioprotective by increasing the tolerance of cardiomyocytes to ischemia, reducing cardiomyocyte apoptosis and increasing prosurvival Akt activation, and (3) MSC-HGF and MSC-VEGF are a valuable source for increased cytokine production and maximize the beneficial effect of MSC-based repair strategies. (Circulation. 2009; 120[suppl 1]: S247-S254.)"],["dc.identifier.doi","10.1161/CIRCULATIONAHA.108.843680"],["dc.identifier.gro","3143055"],["dc.identifier.isi","000269773000035"],["dc.identifier.pmid","19752375"],["dc.identifier.uri","https://resolver.sub.uni-goettingen.de/purl?gro-2/527"],["dc.notes.intern","WoS Import 2017-03-10"],["dc.notes.status","final"],["dc.notes.submitter","PUB_WoS_Import"],["dc.publisher","Lippincott Williams & Wilkins"],["dc.publisher.place","Philadelphia"],["dc.relation.conference","81st Annual Scientific Session of the American-Heart-Association"],["dc.relation.eventlocation","New Orleans, LA"],["dc.relation.ispartof","Circulation"],["dc.relation.issn","0009-7322"],["dc.title","Hepatocyte Growth Factor or Vascular Endothelial Growth Factor Gene Transfer Maximizes Mesenchymal Stem Cell-Based Myocardial Salvage After Acute Myocardial Infarction"],["dc.type","conference_paper"],["dc.type.internalPublication","yes"],["dc.type.peerReviewed","yes"],["dc.type.subtype","original"],["dspace.entity.type","Publication"]]