Schnelle, Moritz Thomas

[["dc.bibliographiccitation.firstpage","H422"],["dc.bibliographiccitation.issue","2"],["dc.bibliographiccitation.journal","American Journal of Physiology-Heart and Circulatory Physiology"],["dc.bibliographiccitation.lastpage","H431"],["dc.bibliographiccitation.volume","319"],["dc.contributor.author","Schnelle, Moritz"],["dc.contributor.author","Chong, Mei"],["dc.contributor.author","Zoccarato, Anna"],["dc.contributor.author","Elkenani, Manar"],["dc.contributor.author","Sawyer, Greta Jane"],["dc.contributor.author","Hasenfuss, Gerd"],["dc.contributor.author","Ludwig, Christian"],["dc.contributor.author","Shah, Ajay M."],["dc.date.accessioned","2021-04-14T08:24:01Z"],["dc.date.available","2021-04-14T08:24:01Z"],["dc.date.issued","2020"],["dc.identifier.doi","10.1152/ajpheart.00219.2020"],["dc.identifier.uri","https://resolver.sub.uni-goettingen.de/purl?gro-2/81138"],["dc.language.iso","en"],["dc.notes.intern","DOI Import GROB-399"],["dc.relation.eissn","1522-1539"],["dc.relation.issn","0363-6135"],["dc.title","In vivo [U- 13 C]glucose labeling to assess heart metabolism in murine models of pressure and volume overload"],["dc.type","journal_article"],["dc.type.internalPublication","yes"],["dspace.entity.type","Publication"]]

[["dc.bibliographiccitation.firstpage","2163"],["dc.bibliographiccitation.issue","22"],["dc.bibliographiccitation.journal","Circulation"],["dc.bibliographiccitation.lastpage","2177"],["dc.bibliographiccitation.volume","135"],["dc.contributor.author","Sag, Can Martin"],["dc.contributor.author","Schnelle, Moritz"],["dc.contributor.author","Zhang, Juqian"],["dc.contributor.author","Murdoch, Colin E."],["dc.contributor.author","Kossmann, Sabine"],["dc.contributor.author","Protti, Andrea"],["dc.contributor.author","Santos, Celio X.C."],["dc.contributor.author","Sawyer, Greta"],["dc.contributor.author","Zhang, Xiaohong"],["dc.contributor.author","Shah, Ajay M."],["dc.date.accessioned","2021-06-01T10:47:48Z"],["dc.date.available","2021-06-01T10:47:48Z"],["dc.date.issued","2017"],["dc.identifier.doi","10.1161/CIRCULATIONAHA.116.023877"],["dc.identifier.uri","https://resolver.sub.uni-goettingen.de/purl?gro-2/85725"],["dc.language.iso","en"],["dc.notes.intern","DOI-Import GROB-425"],["dc.relation.eissn","1524-4539"],["dc.relation.issn","0009-7322"],["dc.title","Distinct Regulatory Effects of Myeloid Cell and Endothelial Cell NAPDH Oxidase 2 on Blood Pressure"],["dc.type","journal_article"],["dc.type.internalPublication","yes"],["dspace.entity.type","Publication"]]

[["dc.bibliographiccitation.firstpage","2090"],["dc.bibliographiccitation.issue","21"],["dc.bibliographiccitation.journal","Circulation"],["dc.bibliographiccitation.lastpage","2091"],["dc.bibliographiccitation.volume","136"],["dc.contributor.author","Sag, Can Martin"],["dc.contributor.author","Schnelle, Moritz"],["dc.contributor.author","Shah, Ajay M."],["dc.date.accessioned","2021-06-01T10:47:49Z"],["dc.date.available","2021-06-01T10:47:49Z"],["dc.date.issued","2017"],["dc.identifier.doi","10.1161/CIRCULATIONAHA.117.030515"],["dc.identifier.uri","https://resolver.sub.uni-goettingen.de/purl?gro-2/85728"],["dc.language.iso","en"],["dc.notes.intern","DOI-Import GROB-425"],["dc.relation.eissn","1524-4539"],["dc.relation.issn","0009-7322"],["dc.title","Response by Sag et al to Letter Regarding Article, “Distinct Regulatory Effects of Myeloid Cell and Endothelial Cell NAPDH Oxidase 2 on Blood Pressure”"],["dc.type","journal_article"],["dc.type.internalPublication","yes"],["dspace.entity.type","Publication"]]

[["dc.bibliographiccitation.firstpage","20"],["dc.bibliographiccitation.journal","Journal of Molecular and Cellular Cardiology"],["dc.bibliographiccitation.lastpage","28"],["dc.bibliographiccitation.volume","114"],["dc.contributor.author","Schnelle, Moritz"],["dc.contributor.author","Catibog, Norman"],["dc.contributor.author","Zhang, Min"],["dc.contributor.author","Nabeebaccus, Adam A."],["dc.contributor.author","Anderson, Grace"],["dc.contributor.author","Richards, Daniel A."],["dc.contributor.author","Sawyer, Greta"],["dc.contributor.author","Zhang, Xiaohong"],["dc.contributor.author","Toischer, Karl"],["dc.contributor.author","Hasenfuss, Gerd"],["dc.contributor.author","Monaghan, Mark J."],["dc.contributor.author","Shah, Ajay M."],["dc.date.accessioned","2018-04-23T11:48:04Z"],["dc.date.available","2018-04-23T11:48:04Z"],["dc.date.issued","2018"],["dc.description.abstract","Background Mouse models of heart disease are extensively employed. The echocardiographic characterization of contractile function is usually focused on systolic function with fewer studies assessing diastolic function. Furthermore, the applicability of diverse echocardiographic parameters of diastolic function that are commonly used in humans has not been extensively evaluated in different pathophysiological models in mice. Methods and results We used high resolution echocardiography to evaluate parameters of diastolic function in mouse models of chronic pressure overload (aortic constriction), volume overload (aorto-caval shunt), heart failure with preserved ejection fraction (HFpEF; DOCA-salt hypertension), and acute sarcoplasmic reticulum dysfunction induced by thapsigargin - all known to exhibit diastolic dysfunction. Left atrial area increased in all three chronic models while mitral E/A was difficult to quantify at high heart rates. Isovolumic relaxation time (IVRT) and Doppler E/E′ increased significantly and the peak longitudinal strain rate during early filling (peak reverse longitudinal strain rate) decreased significantly after aortic constriction, with the changes being proportional to the magnitude of hypertrophy. In the HFpEF model, reverse longitudinal strain rate decreased significantly but changes in IVRT and E/E′ were non-significant, consistent with less severe dysfunction. With volume overload, there was a significant increase in reverse longitudinal strain rate and decrease in IVRT, indicating a restrictive physiology. Acute thapsigargin treatment caused significant prolongation of IVRT and decrease in reverse longitudinal strain rate. Conclusion These results indicate that the combined measurement of left atrial area plus reverse longitudinal strain rate and/or IVRT provide an excellent overall assessment of diastolic function in the diseased mouse heart, allowing distinction between different types of pathophysiology."],["dc.identifier.doi","10.1016/j.yjmcc.2017.10.006"],["dc.identifier.gro","3142326"],["dc.identifier.uri","https://resolver.sub.uni-goettingen.de/purl?gro-2/13460"],["dc.language.iso","en"],["dc.notes.intern","lifescience updates Crossref Import"],["dc.notes.status","final"],["dc.relation.issn","0022-2828"],["dc.title","Echocardiographic evaluation of diastolic function in mouse models of heart disease"],["dc.type","journal_article"],["dc.type.internalPublication","unknown"],["dc.type.peerReviewed","no"],["dspace.entity.type","Publication"]]

[["dc.bibliographiccitation.firstpage","178"],["dc.bibliographiccitation.issue","1"],["dc.bibliographiccitation.journal","Cardiovascular Research"],["dc.bibliographiccitation.lastpage","187"],["dc.bibliographiccitation.volume","117"],["dc.contributor.author","Schnelle, Moritz"],["dc.contributor.author","Sawyer, Iain"],["dc.contributor.author","Anilkumar, Narayana"],["dc.contributor.author","Mohamed, Belal A."],["dc.contributor.author","Richards, Daniel A."],["dc.contributor.author","Toischer, Karl"],["dc.contributor.author","Zhang, Min"],["dc.contributor.author","Catibog, Norman"],["dc.contributor.author","Sawyer, Greta"],["dc.contributor.author","Mongue-Din, Héloïse"],["dc.contributor.author","Schröder, Katrin"],["dc.contributor.author","Hasenfuss, Gerd"],["dc.contributor.author","Shah, Ajay M."],["dc.date.accessioned","2021-04-14T08:30:10Z"],["dc.date.available","2021-04-14T08:30:10Z"],["dc.date.issued","2019"],["dc.description.abstract","Aims\r\n\r\nChronic pressure or volume overload induce concentric vs. eccentric left ventricular (LV) remodelling, respectively. Previous studies suggest that distinct signalling pathways are involved in these responses. NADPH oxidase-4 (Nox4) is a reactive oxygen species-generating enzyme that can limit detrimental cardiac remodelling in response to pressure overload. This study aimed to assess its role in volume overload-induced remodelling.\r\nMethods and results\r\n\r\nWe compared the responses to creation of an aortocaval fistula (Shunt) to induce volume overload in Nox4-null mice (Nox4−/−) vs. wild-type (WT) littermates. Induction of Shunt resulted in a significant increase in cardiac Nox4 mRNA and protein levels in WT mice as compared to Sham controls. Nox4−/− mice developed less eccentric LV remodelling than WT mice (echocardiographic relative wall thickness: 0.30 vs. 0.27, P < 0.05), with less LV hypertrophy at organ level (increase in LV weight/tibia length ratio of 25% vs. 43%, P < 0.01) and cellular level (cardiomyocyte cross-sectional area: 323 µm2 vs. 379 μm2, P < 0.01). LV ejection fraction, foetal gene expression, interstitial fibrosis, myocardial capillary density, and levels of myocyte apoptosis after Shunt were similar in the two genotypes. Myocardial phospho-Akt levels were increased after induction of Shunt in WT mice, whereas levels decreased in Nox4−/− mice (+29% vs. −21%, P < 0.05), associated with a higher level of phosphorylation of the S6 ribosomal protein (S6) and the eIF4E-binding protein 1 (4E-BP1) in WT compared to Nox4−/− mice. We identified that Akt activation in cardiac cells is augmented by Nox4 via a Src kinase-dependent inactivation of protein phosphatase 2A.\r\nConclusion\r\n\r\nEndogenous Nox4 is required for the full development of eccentric cardiac hypertrophy and remodelling during chronic volume overload. Nox4-dependent activation of Akt and its downstream targets S6 and 4E-BP1 may be involved in this effect."],["dc.identifier.doi","10.1093/cvr/cvz331"],["dc.identifier.pmid","31821410"],["dc.identifier.uri","https://resolver.sub.uni-goettingen.de/purl?gro-2/83130"],["dc.identifier.url","https://sfb1002.med.uni-goettingen.de/production/literature/publications/333"],["dc.language.iso","en"],["dc.notes.intern","DOI Import GROB-399"],["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 | D04: Bedeutung der Methylierung von RNA (m6A) und des Histons H3 (H3K4) in der Herzinsuffizienz"],["dc.relation.eissn","1755-3245"],["dc.relation.issn","0008-6363"],["dc.relation.workinggroup","RG Hasenfuß (Transition zur Herzinsuffizienz)"],["dc.relation.workinggroup","RG Toischer (Kardiales Remodeling)"],["dc.rights","CC BY 4.0"],["dc.title","NADPH oxidase-4 promotes eccentric cardiac hypertrophy in response to volume overload"],["dc.type","journal_article"],["dc.type.internalPublication","yes"],["dc.type.subtype","original_ja"],["dc.type.version","published_version"],["dspace.entity.type","Publication"]]