Kessel, Michael

[["dc.bibliographiccitation.artnumber","e001770"],["dc.bibliographiccitation.firstpage","1"],["dc.bibliographiccitation.issue","2"],["dc.bibliographiccitation.journal","Journal of the American Heart Association"],["dc.bibliographiccitation.lastpage","21"],["dc.bibliographiccitation.volume","4"],["dc.contributor.author","Gogiraju, Rajinikanth"],["dc.contributor.author","Xu, Xingbo"],["dc.contributor.author","Bochenek, Magdalena L."],["dc.contributor.author","Steinbrecher, Julia H."],["dc.contributor.author","Lehnart, Stephan E."],["dc.contributor.author","Wenzel, Philip"],["dc.contributor.author","Kessel, Michael"],["dc.contributor.author","Zeisberg, Elisabeth M."],["dc.contributor.author","Dobbelstein, Matthias"],["dc.contributor.author","Schäfer, Katrin"],["dc.date.accessioned","2018-05-07T11:17:45Z"],["dc.date.available","2018-05-07T11:17:45Z"],["dc.date.issued","2015"],["dc.description.abstract","Cardiac dysfunction developing in response to chronic pressure overload is associated with apoptotic cell death and myocardial vessel rarefaction. We examined whether deletion of tumor suppressor p53 in endothelial cells may prevent the transition from cardiac hypertrophy to heart failure."],["dc.identifier.doi","10.1161/JAHA.115.001770"],["dc.identifier.gro","3142397"],["dc.identifier.pmid","25713289"],["dc.identifier.purl","https://resolver.sub.uni-goettingen.de/purl?gs-1/12727"],["dc.identifier.uri","https://resolver.sub.uni-goettingen.de/purl?gro-2/14615"],["dc.identifier.url","https://sfb1002.med.uni-goettingen.de/production/literature/publications/81"],["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 | C01: Epigenetische Kontrolle der Herzfibrose"],["dc.relation","SFB 1002 | C06: Mechanismen und Regulation der koronaren Gefäßneubildung"],["dc.relation.eissn","2047-9980"],["dc.relation.issn","2047-9980"],["dc.relation.issn","2047-9980"],["dc.relation.workinggroup","RG Lehnart (Cellular Biophysics and Translational Cardiology Section)"],["dc.relation.workinggroup","RG Schäfer (Translationale Vaskuläre Biologie)"],["dc.relation.workinggroup","RG E. Zeisberg (Kardiales Stroma)"],["dc.rights","CC BY-NC 4.0"],["dc.rights.uri","https://creativecommons.org/licenses/by-nc/4.0"],["dc.title","Endothelial p53 deletion improves angiogenesis and prevents cardiac fibrosis and heart failure induced by pressure overload in mice"],["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"]]