Schellinger, Isabel N.

[["dc.bibliographiccitation.journal","Frontiers in Physiology"],["dc.bibliographiccitation.volume","9"],["dc.contributor.author","Wagenhäuser, Markus U."],["dc.contributor.author","Schellinger, Isabel N."],["dc.contributor.author","Yoshino, Takuya"],["dc.contributor.author","Toyama, Kensuke"],["dc.contributor.author","Kayama, Yosuke"],["dc.contributor.author","Deng, Alicia"],["dc.contributor.author","Guenther, Sabina P."],["dc.contributor.author","Petzold, Anne"],["dc.contributor.author","Mulorz, Joscha"],["dc.contributor.author","Mulorz, Pireyatharsheny"],["dc.contributor.author","Hasenfuß, Gerd"],["dc.contributor.author","Ibing, Wiebke"],["dc.contributor.author","Elvers, Margitta"],["dc.contributor.author","Schuster, Andreas"],["dc.contributor.author","Ramasubramanian, Anand K."],["dc.contributor.author","Adam, Matti"],["dc.contributor.author","Schelzig, Hubert"],["dc.contributor.author","Spin, Joshua M."],["dc.contributor.author","Raaz, Uwe"],["dc.contributor.author","Tsao, Philip S."],["dc.date.accessioned","2020-12-10T18:44:37Z"],["dc.date.available","2020-12-10T18:44:37Z"],["dc.date.issued","2018"],["dc.identifier.doi","10.3389/fphys.2018.01459"],["dc.identifier.eissn","1664-042X"],["dc.identifier.uri","https://resolver.sub.uni-goettingen.de/purl?gro-2/78531"],["dc.notes.intern","DOI Import GROB-354"],["dc.title","Chronic Nicotine Exposure Induces Murine Aortic Remodeling and Stiffness Segmentation—Implications for Abdominal Aortic Aneurysm Susceptibility"],["dc.type","journal_article"],["dc.type.internalPublication","yes"],["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.firstpage","616"],["dc.bibliographiccitation.issue","3"],["dc.bibliographiccitation.journal","Kidney International"],["dc.bibliographiccitation.lastpage","627"],["dc.bibliographiccitation.volume","91"],["dc.contributor.author","Schellinger, Isabel N."],["dc.contributor.author","Cordasic, Nada"],["dc.contributor.author","Panesar, Julian"],["dc.contributor.author","Buchholz, Bjoern"],["dc.contributor.author","Jacobi, Johannes"],["dc.contributor.author","Hartner, Andrea"],["dc.contributor.author","Klanke, Bernd"],["dc.contributor.author","Jakubiczka-Smorag, Joanna"],["dc.contributor.author","Burzlaff, Nicolai"],["dc.contributor.author","Heinze, Eva"],["dc.contributor.author","Warnecke, Christina"],["dc.contributor.author","Raaz, Uwe"],["dc.contributor.author","Willam, Carsten"],["dc.contributor.author","Tsao, Philip S."],["dc.contributor.author","Eckardt, Kai-Uwe"],["dc.contributor.author","Amann, Kerstin"],["dc.contributor.author","Hilgers, Karl F."],["dc.date.accessioned","2018-11-07T10:26:33Z"],["dc.date.available","2018-11-07T10:26:33Z"],["dc.date.issued","2017"],["dc.description.abstract","Chronic kidney disease (CKD) is associated with increased risk and worse prognosis of cardiovascular disease, including peripheral artery disease. An impaired angiogenic response to ischemia may contribute to poor outcomes of peripheral artery disease in patients with CKD. Hypoxia inducible factors (HIF) are master regulators of angiogenesis and therefore represent a promising target for therapeutic intervention. To test this we induced hind-limb ischemia in rats with CKD caused by 5/6 nephrectomy and administered two different treatments known to stabilize HIF protein in vivo: carbon monoxide and a pharmacological inhibitor of prolyl hydroxylation 2-(1-chloro-4-hydroxyisoquinoline-3-carboxamido) acetate (ICA). Expression levels of proangiogenic HIF target genes (Vegf, Vegf-r1, Vegf-r2, Ho-1) were measured by qRT-PCR. Capillary density was measured by CD31 immunofluorescence staining and HIF expression was evaluated by immunohistochemistry. Capillary density in ischemic skeletal muscle was significantly lower in CKD animals compared to sham controls. Rats with CKD showed significantly lower expression of HIF and all measured pro-angiogenic HIF target genes, including VEGF. Both HIF stabilizing treatments rescued HIF target gene expression in animals with CKD and led to significantly higher ischemia-induced capillary sprouting compared to untreated controls. ICA was effective regardless of whether it was administered before or after induction of ischemia and led to a HIF expression in skeletal muscle. Thus, impaired ischemia-induced angiogenesis in rats with CKD can be improved by HIF stabilization, even if started after onset of ischemia."],["dc.identifier.doi","10.1016/j.kint.2016.09.028"],["dc.identifier.isi","000394921400016"],["dc.identifier.pmid","27927598"],["dc.identifier.uri","https://resolver.sub.uni-goettingen.de/purl?gro-2/43067"],["dc.notes.status","zu prüfen"],["dc.notes.submitter","PUB_WoS_Import"],["dc.publisher","Elsevier Science Inc"],["dc.relation.issn","1523-1755"],["dc.relation.issn","0085-2538"],["dc.title","Hypoxia inducible factor stabilization improves defective ischemia-induced angiogenesis in a rodent model of chronic kidney disease"],["dc.type","journal_article"],["dc.type.internalPublication","yes"],["dc.type.peerReviewed","yes"],["dc.type.status","published"],["dspace.entity.type","Publication"]]

[["dc.bibliographiccitation.firstpage","1796"],["dc.bibliographiccitation.issue","8"],["dc.bibliographiccitation.journal","Arteriosclerosis, Thrombosis, and Vascular Biology"],["dc.bibliographiccitation.lastpage","1805"],["dc.bibliographiccitation.volume","38"],["dc.contributor.author","Adam, Matti"],["dc.contributor.author","Kooreman, Nigel Geoffrey"],["dc.contributor.author","Jagger, Ann"],["dc.contributor.author","Wagenhäuser, Markus U."],["dc.contributor.author","Mehrkens, Dennis"],["dc.contributor.author","Wang, Yongming"],["dc.contributor.author","Kayama, Yosuke"],["dc.contributor.author","Toyama, Kensuke"],["dc.contributor.author","Raaz, Uwe"],["dc.contributor.author","Schellinger, Isabel N."],["dc.contributor.author","Maegdefessel, Lars"],["dc.contributor.author","Spin, Joshua M."],["dc.contributor.author","Hamming, Jaap F."],["dc.contributor.author","Quax, Paul H.A."],["dc.contributor.author","Baldus, Stephan"],["dc.contributor.author","Wu, Joseph C."],["dc.contributor.author","Tsao, Philip S."],["dc.date.accessioned","2020-12-10T18:37:55Z"],["dc.date.available","2020-12-10T18:37:55Z"],["dc.date.issued","2018"],["dc.identifier.doi","10.1161/ATVBAHA.117.310672"],["dc.identifier.eissn","1524-4636"],["dc.identifier.issn","1079-5642"],["dc.identifier.uri","https://resolver.sub.uni-goettingen.de/purl?gro-2/77136"],["dc.language.iso","en"],["dc.notes.intern","DOI Import GROB-354"],["dc.title","Systemic Upregulation of IL-10 (Interleukin-10) Using a Nonimmunogenic Vector Reduces Growth and Rate of Dissecting Abdominal Aortic Aneurysm"],["dc.type","journal_article"],["dc.type.internalPublication","yes"],["dspace.entity.type","Publication"]]

[["dc.bibliographiccitation.journal","Der Internist"],["dc.bibliographiccitation.volume","57"],["dc.contributor.author","Schellinger, Isabel N."],["dc.contributor.author","Tsao, Philip S."],["dc.contributor.author","Hasenfuß, Gerd"],["dc.contributor.author","Raaz, Uwe"],["dc.date.accessioned","2018-11-07T10:15:54Z"],["dc.date.available","2018-11-07T10:15:54Z"],["dc.date.issued","2016"],["dc.format.extent","S75"],["dc.identifier.isi","000375417500148"],["dc.identifier.uri","https://resolver.sub.uni-goettingen.de/purl?gro-2/40915"],["dc.notes.status","zu prüfen"],["dc.notes.submitter","Najko"],["dc.publisher","Springer"],["dc.publisher.place","New york"],["dc.relation.issn","1432-1289"],["dc.relation.issn","0020-9554"],["dc.title","Transcription factor Runx2 is induced in vascular aging and may promote age-related arterial stiffness"],["dc.type","conference_abstract"],["dc.type.internalPublication","yes"],["dc.type.peerReviewed","yes"],["dc.type.status","published"],["dspace.entity.type","Publication"]]

[["dc.bibliographiccitation.firstpage","513"],["dc.bibliographiccitation.issue","6"],["dc.bibliographiccitation.journal","Circulation Research"],["dc.bibliographiccitation.lastpage","524"],["dc.bibliographiccitation.volume","117"],["dc.contributor.author","Raaz, Uwe"],["dc.contributor.author","Schellinger, Isabel N."],["dc.contributor.author","Chernogubova, Ekaterina"],["dc.contributor.author","Warnecke, Christina"],["dc.contributor.author","Kayama, Yosuke"],["dc.contributor.author","Penov, Kiril"],["dc.contributor.author","Hennigs, Jan K."],["dc.contributor.author","Salomons, Florian"],["dc.contributor.author","Eken, Suzanne"],["dc.contributor.author","Emrich, Fabian C."],["dc.contributor.author","Zheng, Wei H."],["dc.contributor.author","Adam, Matti"],["dc.contributor.author","Jagger, Ann"],["dc.contributor.author","Nakagami, Futoshi"],["dc.contributor.author","Toh, Ryuji"],["dc.contributor.author","Toyama, Kensuke"],["dc.contributor.author","Deng, Alicia"],["dc.contributor.author","Buerke, Michael"],["dc.contributor.author","Maegdefessel, Lars"],["dc.contributor.author","Hasenfuß, Gerd"],["dc.contributor.author","Spin, Joshua M."],["dc.contributor.author","Tsao, Philip S."],["dc.date.accessioned","2017-09-07T11:43:37Z"],["dc.date.available","2017-09-07T11:43:37Z"],["dc.date.issued","2015"],["dc.description.abstract","Rationale: Accelerated arterial stiffening is a major complication of diabetes mellitus with no specific therapy available to date. Objective: The present study investigates the role of the osteogenic transcription factor runt-related transcription factor 2 (Runx2) as a potential mediator and therapeutic target of aortic fibrosis and aortic stiffening in diabetes mellitus. Methods and Results: Using a murine model of type 2 diabetes mellitus (db/db mice), we identify progressive structural aortic stiffening that precedes the onset of arterial hypertension. At the same time, Runx2 is aberrantly upregulated in the medial layer of db/db aortae, as well as in thoracic aortic samples from patients with type 2 diabetes mellitus. Vascular smooth muscle cell-specific overexpression of Runx2 in transgenic mice increases expression of its target genes, Col1a1 and Col1a2, leading to medial fibrosis and aortic stiffening. Interestingly, increased Runx2 expression per se is not sufficient to induce aortic calcification. Using in vivo and in vitro approaches, we further demonstrate that expression of Runx2 in diabetes mellitus is regulated via a redox-sensitive pathway that involves a direct interaction of NF-B with the Runx2 promoter. Conclusions: In conclusion, this study highlights Runx2 as a previously unrecognized inducer of vascular fibrosis in the setting of diabetes mellitus, promoting arterial stiffness irrespective of calcification."],["dc.identifier.doi","10.1161/CIRCRESAHA.115.306341"],["dc.identifier.gro","3141842"],["dc.identifier.isi","000360142000007"],["dc.identifier.pmid","26208651"],["dc.identifier.uri","https://resolver.sub.uni-goettingen.de/purl?gro-2/1679"],["dc.notes.intern","WoS Import 2017-03-10"],["dc.notes.status","final"],["dc.notes.submitter","PUB_WoS_Import"],["dc.publisher","Lippincott Williams & Wilkins"],["dc.relation.eissn","1524-4571"],["dc.relation.issn","0009-7330"],["dc.title","Transcription Factor Runx2 Promotes Aortic Fibrosis and Stiffness in Type 2 Diabetes Mellitus"],["dc.type","journal_article"],["dc.type.internalPublication","yes"],["dc.type.peerReviewed","yes"],["dc.type.subtype","original"],["dspace.entity.type","Publication"]]

[["dc.bibliographiccitation.journal","Der Internist"],["dc.bibliographiccitation.volume","57"],["dc.contributor.author","Raaz, Uwe"],["dc.contributor.author","Schellinger, Isabel N."],["dc.contributor.author","Maegdefessel, Lars"],["dc.contributor.author","Spin, Joshua M."],["dc.contributor.author","Hasenfuß, Gerd"],["dc.contributor.author","Tsao, Philip S."],["dc.date.accessioned","2018-11-07T10:15:54Z"],["dc.date.available","2018-11-07T10:15:54Z"],["dc.date.issued","2016"],["dc.format.extent","S58"],["dc.identifier.isi","000375417500113"],["dc.identifier.uri","https://resolver.sub.uni-goettingen.de/purl?gro-2/40914"],["dc.notes.status","zu prüfen"],["dc.notes.submitter","Najko"],["dc.publisher","Springer"],["dc.publisher.place","New york"],["dc.relation.issn","1432-1289"],["dc.relation.issn","0020-9554"],["dc.title","MicroRNA miR-29b is a mediator of aortic stiffness and hypertension in a murine model of diabetes mellitus type 2"],["dc.type","conference_abstract"],["dc.type.internalPublication","yes"],["dc.type.peerReviewed","yes"],["dc.type.status","published"],["dspace.entity.type","Publication"]]

[["dc.bibliographiccitation.firstpage","633"],["dc.bibliographiccitation.issue","4"],["dc.bibliographiccitation.journal","Circulation Research"],["dc.bibliographiccitation.lastpage","644"],["dc.bibliographiccitation.volume","120"],["dc.contributor.author","Eken, Suzanne M."],["dc.contributor.author","Jin, Hong"],["dc.contributor.author","Chernogubova, Ekaterina"],["dc.contributor.author","Li, Yuhuang"],["dc.contributor.author","Simon, Nancy"],["dc.contributor.author","Sun, Changyan"],["dc.contributor.author","Korzunowicz, Greg"],["dc.contributor.author","Busch, Albert"],["dc.contributor.author","Bäcklund, Alexandra"],["dc.contributor.author","Österholm, Cecilia"],["dc.contributor.author","Razuvaev, Anton"],["dc.contributor.author","Renné, Thomas"],["dc.contributor.author","Eckstein, Hans Henning"],["dc.contributor.author","Pelisek, Jaroslav"],["dc.contributor.author","Eriksson, Per"],["dc.contributor.author","González Díez, María"],["dc.contributor.author","Perisic Matic, Ljubica"],["dc.contributor.author","Schellinger, Isabel N."],["dc.contributor.author","Raaz, Uwe"],["dc.contributor.author","Leeper, Nicholas J."],["dc.contributor.author","Hansson, Göran K."],["dc.contributor.author","Paulsson-Berne, Gabrielle"],["dc.contributor.author","Hedin, Ulf"],["dc.contributor.author","Maegdefessel, Lars"],["dc.date.accessioned","2020-12-10T18:37:59Z"],["dc.date.available","2020-12-10T18:37:59Z"],["dc.date.issued","2017"],["dc.description.abstract","Rationale: In the search for markers and modulators of vascular disease, microRNAs (miRNAs) have emerged as potent therapeutic targets. Objective: To investigate miRNAs of clinical interest in patients with unstable carotid stenosis at risk of stroke. Methods and Results: Using patient material from the BiKE (Biobank of Karolinska Endarterectomies), we profiled miRNA expression in patients with stable versus unstable carotid plaque. A polymerase chain reactionbased miRNA array of plasma, sampled at the carotid lesion site, identified 8 deregulated miRNAs (miR-15b, miR29c, miR-30c/d, miR-150, miR-191, miR-210, and miR-500). miR-210 was the most significantly downregulated miRNA in local plasma material. Laser capture microdissection and in situ hybridization revealed a distinct localization of miR-210 in fibrous caps. We confirmed that miR-210 directly targets the tumor suppressor gene APC (adenomatous polyposis coli), thereby affecting Wnt (Wingless-related integration site) signaling and regulating smooth muscle cell survival, as well as differentiation in advanced atherosclerotic lesions. Substantial changes in arterial miR-210 were detectable in 2 rodent models of vascular remodeling and plaque rupture. Modulating miR210 in vitro and in vivo improved fibrous cap stability with implications for vascular disease. Conclusions: An unstable carotid plaque at risk of stroke is characterized by low expression of miR-210. miR-210 contributes to stabilizing carotid plaques through inhibition of APC, ensuring smooth muscle cell survival. We present local delivery of miR-210 as a therapeutic approach for prevention of atherothrombotic vascular events."],["dc.identifier.doi","10.1161/CIRCRESAHA.116.309318"],["dc.identifier.eissn","1524-4571"],["dc.identifier.isi","000394446200016"],["dc.identifier.issn","0009-7330"],["dc.identifier.pmid","27895035"],["dc.identifier.uri","https://resolver.sub.uni-goettingen.de/purl?gro-2/77157"],["dc.language.iso","en"],["dc.notes.intern","DOI Import GROB-354"],["dc.notes.status","zu prüfen"],["dc.notes.submitter","PUB_WoS_Import"],["dc.publisher","Lippincott Williams & Wilkins"],["dc.relation.issn","1524-4571"],["dc.relation.issn","0009-7330"],["dc.title","MicroRNA-210 Enhances Fibrous Cap Stability in Advanced Atherosclerotic Lesions"],["dc.type","journal_article"],["dc.type.internalPublication","yes"],["dc.type.peerReviewed","yes"],["dc.type.status","published"],["dspace.entity.type","Publication"]]

[["dc.bibliographiccitation.firstpage","E11"],["dc.bibliographiccitation.issue","1"],["dc.bibliographiccitation.journal","Circulation"],["dc.bibliographiccitation.lastpage","E12"],["dc.bibliographiccitation.volume","133"],["dc.contributor.author","Raaz, Uwe"],["dc.contributor.author","Zöllner, Alexander M."],["dc.contributor.author","Schellinger, Isabel N."],["dc.contributor.author","Toh, Ryuji"],["dc.contributor.author","Nakagami, Futoshi"],["dc.contributor.author","Brandt, Moritz"],["dc.contributor.author","Emrich, Fabian C."],["dc.contributor.author","Kayama, Yosuke"],["dc.contributor.author","Eken, Suzanne"],["dc.contributor.author","Adam, Matti"],["dc.contributor.author","Maegdefessel, Lars"],["dc.contributor.author","Hertel, Thomas"],["dc.contributor.author","Deng, Alicia"],["dc.contributor.author","Jagger, Ann"],["dc.contributor.author","Buerke, Michael"],["dc.contributor.author","Dalman, Ronald L."],["dc.contributor.author","Spin, Joshua M."],["dc.contributor.author","Kuhl, Ellen"],["dc.contributor.author","Tsao, Philip S."],["dc.date.accessioned","2020-12-10T18:38:00Z"],["dc.date.available","2020-12-10T18:38:00Z"],["dc.date.issued","2016"],["dc.identifier.doi","10.1161/CIRCULATIONAHA.115.018759"],["dc.identifier.eissn","1524-4539"],["dc.identifier.isi","000367540000006"],["dc.identifier.issn","0009-7322"],["dc.identifier.pmid","26719393"],["dc.identifier.uri","https://resolver.sub.uni-goettingen.de/purl?gro-2/77164"],["dc.language.iso","en"],["dc.notes.intern","DOI Import GROB-354"],["dc.notes.status","zu prüfen"],["dc.notes.submitter","Najko"],["dc.publisher","Lippincott Williams & Wilkins"],["dc.relation.issn","1524-4539"],["dc.relation.issn","0009-7322"],["dc.title","Response to Letters Regarding Article, \"Segmental Aortic Stiffening Contributes to Experimental Abdominal Aortic Aneurysm Development\""],["dc.type","journal_article"],["dc.type.internalPublication","yes"],["dc.type.peerReviewed","yes"],["dc.type.status","published"],["dc.type.subtype","letter_note"],["dspace.entity.type","Publication"]]

[["dc.bibliographiccitation.issue","Suppl_1"],["dc.bibliographiccitation.journal","Arteriosclerosis, Thrombosis, and Vascular Biology"],["dc.bibliographiccitation.volume","38"],["dc.contributor.author","Dannert, Angelika"],["dc.contributor.author","Schellinger, Isabel N"],["dc.contributor.author","Jakubiczka-Smorag, Joanna"],["dc.contributor.author","Mattern, Karin"],["dc.contributor.author","Petzold, Anne"],["dc.contributor.author","Hasenfuss, Gerd"],["dc.contributor.author","Raaz, Uwe"],["dc.date.accessioned","2020-12-10T18:37:54Z"],["dc.date.available","2020-12-10T18:37:54Z"],["dc.date.issued","2018"],["dc.identifier.doi","10.1161/atvb.38.suppl_1.678"],["dc.identifier.eissn","1524-4636"],["dc.identifier.issn","1079-5642"],["dc.identifier.uri","https://resolver.sub.uni-goettingen.de/purl?gro-2/77134"],["dc.language.iso","en"],["dc.notes.intern","DOI Import GROB-354"],["dc.title","Abstract 678: microRNA 146a Reduces Activity of Matrix-Metalloproteinases in the Context of Arterial Stiffness"],["dc.type","journal_article"],["dc.type.internalPublication","yes"],["dspace.entity.type","Publication"]]