Zimmermann, Wolfram-Hubertus

[["dc.bibliographiccitation.firstpage","272"],["dc.bibliographiccitation.issue","3"],["dc.bibliographiccitation.journal","European Journal of Heart Failure"],["dc.bibliographiccitation.lastpage","285"],["dc.bibliographiccitation.volume","21"],["dc.contributor.author","de Boer, Rudolf A."],["dc.contributor.author","De Keulenaer, Gilles"],["dc.contributor.author","Bauersachs, Johann"],["dc.contributor.author","Brutsaert, Dirk"],["dc.contributor.author","Cleland, John G."],["dc.contributor.author","Diez, Javier"],["dc.contributor.author","Du, Xiao‐Jun"],["dc.contributor.author","Ford, Paul"],["dc.contributor.author","Heinzel, Frank R."],["dc.contributor.author","Lipson, Kenneth E."],["dc.contributor.author","McDonagh, Theresa"],["dc.contributor.author","Lopez‐Andres, Natalia"],["dc.contributor.author","Lunde, Ida G."],["dc.contributor.author","Lyon, Alexander R."],["dc.contributor.author","Pollesello, Piero"],["dc.contributor.author","Prasad, Sanjay K."],["dc.contributor.author","Tocchetti, Carlo G."],["dc.contributor.author","Mayr, Manuel"],["dc.contributor.author","Sluijter, Joost P.G."],["dc.contributor.author","Thum, Thomas"],["dc.contributor.author","Tschöpe, Carsten"],["dc.contributor.author","Zannad, Faiez"],["dc.contributor.author","Zimmermann, Wolfram-Hubertus"],["dc.contributor.author","Ruschitzka, Frank"],["dc.contributor.author","Filippatos, Gerasimos"],["dc.contributor.author","Lindsey, Merry L."],["dc.contributor.author","Maack, Christoph"],["dc.contributor.author","Heymans, Stephane"],["dc.date.accessioned","2019-07-09T11:50:51Z"],["dc.date.available","2019-07-09T11:50:51Z"],["dc.date.issued","2019"],["dc.description.abstract","Fibrosis is a pivotal player in heart failure development and progression. Measurements of (markers of) fibrosis in tissue and blood may help to diagnose and risk stratify patients with heart failure, and its treatment may be effective in preventing heart failure and its progression. A lack of pathophysiological insights and uniform definitions has hampered the research in fibrosis and heart failure. The Translational Research Committee of the Heart Failure Association discussed several aspects of fibrosis in their workshop. Early insidious perturbations such as subclinical hypertension or inflammation may trigger first fibrotic events, while more dramatic triggers such as myocardial infarction and myocarditis give rise to full blown scar formation and ongoing fibrosis in diseased hearts. Aging itself is also associated with a cardiac phenotype that includes fibrosis. Fibrosis is an extremely heterogeneous phenomenon, as several stages of the fibrotic process exist, each with different fibrosis subtypes and a different composition of various cells and proteins - resulting in a very complex pathophysiology. As a result, detection of fibrosis, e.g. using current cardiac imaging modalities or plasma biomarkers, will detect only specific subforms of fibrosis, but cannot capture all aspects of the complex fibrotic process. Furthermore, several anti-fibrotic therapies are under investigation, but such therapies generally target aspecific aspects of the fibrotic process and suffer from a lack of precision. This review discusses the mechanisms and the caveats and proposes a roadmap for future research."],["dc.identifier.doi","10.1002/ejhf.1406"],["dc.identifier.pmid","30714667"],["dc.identifier.purl","https://resolver.sub.uni-goettingen.de/purl?gs-1/16014"],["dc.identifier.uri","https://resolver.sub.uni-goettingen.de/purl?gro-2/59843"],["dc.language.iso","en"],["dc.notes.intern","Merged from goescholar"],["dc.relation","info:eu-repo/grantAgreement/EC/FP7/305507/EU//HOMAGE"],["dc.relation","info:eu-repo/grantAgreement/EC/FP7/602904/EU//FIBRO-TARGETS"],["dc.relation","info:eu-repo/grantAgreement/EC/FP7/602156/EU//HECATOS"],["dc.rights","CC BY-NC 4.0"],["dc.rights.uri","https://creativecommons.org/licenses/by-nc/4.0"],["dc.subject.ddc","610"],["dc.title","Towards better definition, quantification and treatment of fibrosis in heart failure. A scientific roadmap by the Committee of Translational Research of the Heart Failure Association (HFA) of the European Society of Cardiology"],["dc.type","journal_article"],["dc.type.internalPublication","yes"],["dc.type.version","published_version"],["dspace.entity.type","Publication"]]

[["dc.bibliographiccitation.artnumber","2665"],["dc.bibliographiccitation.journal","Frontiers in Immunology"],["dc.bibliographiccitation.volume","9"],["dc.contributor.author","Gröschel, Carina"],["dc.contributor.author","Sasse, André"],["dc.contributor.author","Monecke, Sebastian"],["dc.contributor.author","Röhrborn, Charlotte"],["dc.contributor.author","Elsner, Leslie"],["dc.contributor.author","Didié, Michael"],["dc.contributor.author","Reupke, Verena"],["dc.contributor.author","Bunt, Gertrude"],["dc.contributor.author","Lichtman, Andrew H."],["dc.contributor.author","Toischer, Karl"],["dc.contributor.author","Zimmermann, Wolfram-Hubertus"],["dc.contributor.author","Hasenfuß, Gerd"],["dc.contributor.author","Dressel, Ralf"],["dc.date.accessioned","2019-07-09T11:49:35Z"],["dc.date.available","2019-07-09T11:49:35Z"],["dc.date.issued","2018"],["dc.description.abstract","Heart failure due to pressure overload is frequently associated with inflammation. In addition to inflammatory responses of the innate immune system, autoimmune reactions of the adaptive immune system appear to be triggered in subgroups of patients with heart failure as demonstrated by the presence of autoantibodies against myocardial antigens. Moreover, T cell-deficient and T cell-depleted mice have been reported to be protected from heart failure induced by transverse aortic constriction (TAC) and we have shown recently that CD4+-helper T cells with specificity for an antigen in cardiomyocytes accelerate TAC-induced heart failure. In this study, we set out to investigate the potential contribution of CD8+-cytotoxic T cells with specificity to a model antigen (ovalbumin, OVA) in cardiomyocytes to pressure overload-induced heart failure. In 78% of cMy-mOVA mice with cardiomyocyte-specific OVA expression, a low-grade OVA-specific cellular cytotoxicity was detected after TAC. Adoptive transfer of OVA-specific CD8+-T cells from T cell receptor transgenic OT-I mice before TAC did not increase the risk of OVA-specific autoimmunity in cMy-mOVA mice. After TAC, again 78% of the mice displayed an OVA-specific cytotoxicity with on average only a three-fold higher killing of OVA-expressing target cells. More CD8+ cells were present after TAC in the myocardium of cMy-mOVA mice with OT-I T cells (on average 17.5/mm2) than in mice that did not receive OVA-specific CD8+-T cells (3.6/mm2). However, the extent of fibrosis was similar in both groups. Functionally, as determined by echocardiography, the adoptive transfer of OVA-specific CD8+-T cells did not significantly accelerate the progression from hypertrophy to heart failure in cMy-mOVA mice. These findings argue therefore against a major impact of cytotoxic T cells with specificity for autoantigens of cardiomyocytes in pressure overload-induced heart failure."],["dc.identifier.doi","10.3389/fimmu.2018.02665"],["dc.identifier.pmid","30498501"],["dc.identifier.purl","https://resolver.sub.uni-goettingen.de/purl?gs-1/15720"],["dc.identifier.uri","https://resolver.sub.uni-goettingen.de/purl?gro-2/59587"],["dc.identifier.url","https://sfb1002.med.uni-goettingen.de/production/literature/publications/298"],["dc.language.iso","en"],["dc.notes.intern","Merged from goescholar"],["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 | C04: Fibroblasten-Kardiomyozyten Interaktion im gesunden und erkrankten Herzen: Mechanismen und therapeutische Interventionen bei Kardiofibroblastopathien"],["dc.relation","SFB 1002 | C05: Bedeutung von zellulären Immunreaktionen für das kardiale Remodeling und die Therapie der Herzinsuffizienz durch Stammzelltransplantation"],["dc.relation","SFB 1002 | S01: In vivo und in vitro Krankheitsmodelle"],["dc.relation.workinggroup","RG Dressel"],["dc.relation.workinggroup","RG Hasenfuß (Transition zur Herzinsuffizienz)"],["dc.relation.workinggroup","RG Toischer (Kardiales Remodeling)"],["dc.relation.workinggroup","RG Zimmermann (Engineered Human Myocardium)"],["dc.rights","CC BY 4.0"],["dc.rights.uri","https://creativecommons.org/licenses/by/4.0"],["dc.subject.ddc","610"],["dc.title","CD8+-T Cells With Specificity for a Model Antigen in Cardiomyocytes Can Become Activated After Transverse Aortic Constriction but Do Not Accelerate Progression to 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.firstpage","731"],["dc.bibliographiccitation.issue","12"],["dc.bibliographiccitation.journal","FASEB BioAdvances"],["dc.bibliographiccitation.lastpage","746"],["dc.bibliographiccitation.volume","1"],["dc.contributor.author","Tiburcy, Malte"],["dc.contributor.author","Markov, Alex"],["dc.contributor.author","Kraemer, Lena K."],["dc.contributor.author","Christalla, Peter"],["dc.contributor.author","Rave-Fränk, Margret"],["dc.contributor.author","Fischer, Henrike J."],["dc.contributor.author","Reichardt, Holger Michael"],["dc.contributor.author","Zimmermann, Wolfram-Hubertus"],["dc.date.accessioned","2020-01-21T09:29:21Z"],["dc.date.accessioned","2021-10-27T13:22:07Z"],["dc.date.available","2020-01-21T09:29:21Z"],["dc.date.available","2021-10-27T13:22:07Z"],["dc.date.issued","2019"],["dc.description.abstract","Satellite cells reside in defined niches and are activated upon skeletal muscle injury to facilitate regeneration. Mechanistic studies of skeletal muscle regeneration are hampered by the inability to faithfully simulate satellite cell biology in vitro. We sought to overcome this limitation by developing tissue engineered skeletal muscle (ESM) with (1) satellite cell niches and (2) the capacity to regenerate after injury. ESMs contained quiescent Pax7‐positive satellite cells in morphologically defined niches. Satellite cells could be activated to repair (i) cardiotoxin and (ii) mechanical crush injuries. Activation of the Wnt‐pathway was essential for muscle regeneration. Finally, muscle progenitors from the engineered niche developed de novo ESM in vitro and regenerated skeletal muscle after cardiotoxin‐induced injury in vivo. We conclude that ESM with functional progenitor niches reminiscent of the in vivo satellite cell niches can be engineered in vitro. ESM may ultimately be exploited in disease modeling, drug screening, or muscle regeneration."],["dc.description.sponsorship","Open-Access-Publikationsfonds 2019"],["dc.identifier.doi","10.1096/fba.2019-00013"],["dc.identifier.purl","https://resolver.sub.uni-goettingen.de/purl?gs-1/17135"],["dc.identifier.uri","https://resolver.sub.uni-goettingen.de/purl?gro-2/92070"],["dc.language.iso","en"],["dc.notes.intern","Migrated from goescholar"],["dc.relation.eissn","2573-9832"],["dc.relation.issn","2573-9832"],["dc.relation.issn","2573-9832"],["dc.relation.orgunit","Universitätsmedizin Göttingen"],["dc.rights","CC BY 4.0"],["dc.rights.uri","https://creativecommons.org/licenses/by/4.0"],["dc.subject.ddc","610"],["dc.title","Regeneration competent satellite cell niches in rat engineered skeletal muscle"],["dc.type","journal_article"],["dc.type.internalPublication","yes"],["dc.type.peerReviewed","yes"],["dc.type.version","published_version"],["dspace.entity.type","Publication"]]

[["dc.bibliographiccitation.artnumber","5651"],["dc.bibliographiccitation.issue","1"],["dc.bibliographiccitation.journal","Scientific Reports"],["dc.bibliographiccitation.volume","9"],["dc.contributor.author","Sattler, Katherine"],["dc.contributor.author","El-Battrawy, Ibrahim"],["dc.contributor.author","Zhao, Zhihan"],["dc.contributor.author","Schrottenberg, Christoph"],["dc.contributor.author","Yücel, Gökhan"],["dc.contributor.author","Lan, Huan"],["dc.contributor.author","Li, Xin"],["dc.contributor.author","Lang, Siegfried"],["dc.contributor.author","Zimmermann, Wolfram-Hubertus"],["dc.contributor.author","Cyganek, Lukas"],["dc.contributor.author","Utikal, Jochen"],["dc.contributor.author","Wieland, Thomas"],["dc.contributor.author","Ravens, Ursula"],["dc.contributor.author","Bieback, Karen"],["dc.contributor.author","Borggrefe, Martin"],["dc.contributor.author","Zhou, Xiaobo"],["dc.contributor.author","Akin, Ibrahim"],["dc.date.accessioned","2019-07-09T11:51:39Z"],["dc.date.available","2019-07-09T11:51:39Z"],["dc.date.issued","2019"],["dc.description.abstract","Acute myocardial infarction (MI) evokes a systemic inflammatory response and locally the degradation of the necrotic tissue, followed by scar formation. The mechanisms for containment of the infarct zone are not studied well. The study aimed to examine the response of healthy cardiomyocytes to serum of patients with myocardial infarction. Human iPSC-cardiomyocytes (iPSC-CM) generated from two healthy donors were incubated with serum of patients with MI with and without ventricular fibrillation (VF) or of healthy controls. Different cell adhesion molecules were studied by flow cytometry and immunostaining. Cellular electrophysiology was studied by patch clamp. The cell adhesion molecules CD54/ICAM-1, CD58/LFA-3 and CD321/JAM-A were expressed on iPSC-CM within the plasma membrane. Incubation with serum of MI patients reduced the levels of expression of CD54/ICAM-1 and CD321/JAM-A by 15-20%. VF serum was less effective than serum of MI patients without VF. MI serum or VF serum did not affect resting potential, action potential duration or maximum depolarization velocity. Myocardial infarction serum exerts anti-inflammatory effects on healthy cardiomyocytes without affecting their electrical activity, thus helping to contain the infarct zone and to protect healthy tissue. Ventricular fibrillation during MI drives healthy cardiomyocytes towards a pro-inflammatory phenotype."],["dc.identifier.doi","10.1038/s41598-019-42079-z"],["dc.identifier.pmid","30948775"],["dc.identifier.purl","https://resolver.sub.uni-goettingen.de/purl?gs-1/16161"],["dc.identifier.uri","https://resolver.sub.uni-goettingen.de/purl?gro-2/59980"],["dc.identifier.url","https://sfb1002.med.uni-goettingen.de/production/literature/publications/327"],["dc.language.iso","en"],["dc.notes.intern","Merged from goescholar"],["dc.rights","CC BY 4.0"],["dc.rights.uri","https://creativecommons.org/licenses/by/4.0"],["dc.subject.ddc","610"],["dc.title","Serum of patients with acute myocardial infarction prevents inflammation in iPSC-cardiomyocytes"],["dc.type","journal_article"],["dc.type.internalPublication","yes"],["dc.type.subtype","original_ja"],["dc.type.version","published_version"],["dspace.entity.type","Publication"]]