Pabel, Steffen

[["dc.bibliographiccitation.firstpage","1111"],["dc.bibliographiccitation.issue","7"],["dc.bibliographiccitation.journal","Europace"],["dc.bibliographiccitation.lastpage","1118"],["dc.bibliographiccitation.volume","22"],["dc.contributor.author","Pabel, Steffen"],["dc.contributor.author","Mustroph, Julian"],["dc.contributor.author","Stehle, Thea"],["dc.contributor.author","Lebek, Simon"],["dc.contributor.author","Dybkova, Nataliya"],["dc.contributor.author","Keyser, Andreas"],["dc.contributor.author","Rupprecht, Leopold"],["dc.contributor.author","Wagner, Stefan"],["dc.contributor.author","Neef, Stefan"],["dc.contributor.author","Maier, Lars S"],["dc.contributor.author","Sossalla, Samuel"],["dc.date.accessioned","2021-04-14T08:24:15Z"],["dc.date.available","2021-04-14T08:24:15Z"],["dc.date.issued","2020"],["dc.identifier.doi","10.1093/europace/euaa079"],["dc.identifier.uri","https://resolver.sub.uni-goettingen.de/purl?gro-2/81221"],["dc.language.iso","en"],["dc.notes.intern","DOI Import GROB-399"],["dc.relation.eissn","1532-2092"],["dc.relation.issn","1099-5129"],["dc.title","Dantrolene reduces CaMKIIδC-mediated atrial arrhythmias"],["dc.type","journal_article"],["dc.type.internalPublication","yes"],["dspace.entity.type","Publication"]]

[["dc.bibliographiccitation.firstpage","1689"],["dc.bibliographiccitation.issue","12"],["dc.bibliographiccitation.journal","Journal of Molecular Medicine"],["dc.bibliographiccitation.lastpage","1700"],["dc.bibliographiccitation.volume","98"],["dc.contributor.author","Pabel, Steffen"],["dc.contributor.author","Reetz, Florian"],["dc.contributor.author","Dybkova, Nataliya"],["dc.contributor.author","Shomroni, Orr"],["dc.contributor.author","Salinas, Gabriela"],["dc.contributor.author","Mustroph, Julian"],["dc.contributor.author","Hammer, Karin P."],["dc.contributor.author","Hasenfuss, Gerd"],["dc.contributor.author","Hamdani, Nazha"],["dc.contributor.author","Maier, Lars S."],["dc.contributor.author","Streckfuss-Bömeke, Katrin"],["dc.contributor.author","Sossalla, Samuel"],["dc.date.accessioned","2021-04-14T08:32:15Z"],["dc.date.available","2021-04-14T08:32:15Z"],["dc.date.issued","2020"],["dc.identifier.doi","10.1007/s00109-020-01989-6"],["dc.identifier.uri","https://resolver.sub.uni-goettingen.de/purl?gro-2/83859"],["dc.language.iso","en"],["dc.notes.intern","DOI Import GROB-399"],["dc.relation.eissn","1432-1440"],["dc.relation.issn","0946-2716"],["dc.title","Long-term effects of empagliflozin on excitation-contraction-coupling in human induced pluripotent stem cell cardiomyocytes"],["dc.type","journal_article"],["dc.type.internalPublication","yes"],["dspace.entity.type","Publication"]]

[["dc.bibliographiccitation.firstpage","1673"],["dc.bibliographiccitation.issue","12"],["dc.bibliographiccitation.journal","European Journal of Heart Failure"],["dc.bibliographiccitation.lastpage","1685"],["dc.bibliographiccitation.volume","20"],["dc.contributor.author","Fischer, Thomas H."],["dc.contributor.author","Eiringhaus, Jörg"],["dc.contributor.author","Dybkova, Nataliya"],["dc.contributor.author","Saadatmand, Alireza"],["dc.contributor.author","Pabel, Steffen"],["dc.contributor.author","Weber, Silvio"],["dc.contributor.author","Wang, Yansong"],["dc.contributor.author","Köhn, Maja"],["dc.contributor.author","Tirilomis, Theodor"],["dc.contributor.author","Ljubojevic, Senka"],["dc.contributor.author","Renner, André"],["dc.contributor.author","Gummert, Jan"],["dc.contributor.author","Maier, Lars S."],["dc.contributor.author","Hasenfuß, Gerd"],["dc.contributor.author","El-Armouche, Ali"],["dc.contributor.author","Sossalla, Samuel"],["dc.date.accessioned","2019-02-18T13:43:31Z"],["dc.date.available","2019-02-18T13:43:31Z"],["dc.date.issued","2018"],["dc.description.abstract","Background Disruption of Ca2+ homeostasis is a key pathomechanism in heart failure. CaMKII-dependent hyperphosphorylation of ryanodine receptors in the sarcoplasmic reticulum (SR) increases the arrhythmogenic SR Ca2+ leak and depletes SR Ca2+ stores. The contribution of conversely acting serine/threonine phosphatases [protein phosphatase 1 (PP1) and 2A (PP2A)] is largely unknown. Methods and results Human myocardium from three groups of patients was investigated: (i) healthy controls (non-failing, NF, n = 8), (ii) compensated hypertrophy (Hy, n = 16), and (iii) end-stage heart failure (HF, n = 52). Expression of PP1 was unchanged in Hy but greater in HF compared to NF while its endogenous inhibitor-1 (I-1) was markedly lower expressed in both compared to NF, suggesting increased total PP1 activity. In contrast, PP2A expression was lower in Hy and HF compared to NF. Ca2+ homeostasis was severely disturbed in HF compared to Hy signified by a higher SR Ca2+ leak, lower systolic Ca2+ transients as well as a decreased SR Ca2+ load. Inhibition of PP1/PP2A by okadaic acid increased SR Ca2+ load and systolic Ca2+ transients but severely aggravated diastolic SR Ca2+ leak and cellular arrhythmias in Hy. Conversely, selective activation of PP1 by a PP1-disrupting peptide (PDP3) in HF potently reduced SR Ca2+ leak as well as cellular arrhythmias and, importantly, did not compromise systolic Ca2+ release and SR Ca2+ load. Conclusion This study is the first to functionally investigate the role of PP1/PP2A for Ca2+ homeostasis in diseased human myocardium. Our data indicate that a modulation of phosphatase activity potently impacts Ca2+ cycling properties. An activation of PP1 counteracts increased kinase activity in heart failure and successfully seals the arrhythmogenic SR Ca2+ leak. It may thus represent a promising future antiarrhythmic therapeutic approach."],["dc.identifier.doi","10.1002/ejhf.1297"],["dc.identifier.pmid","30191648"],["dc.identifier.uri","https://resolver.sub.uni-goettingen.de/purl?gro-2/57579"],["dc.identifier.url","https://sfb1002.med.uni-goettingen.de/production/literature/publications/232"],["dc.language.iso","en"],["dc.notes.status","final"],["dc.relation","SFB 1002: Modulatorische Einheiten bei Herzinsuffizienz"],["dc.relation","SFB 1002 | A11: Absolute Arrhythmie bei Vorhofflimmern - ein neuer Mechanismus, der zu einer Störung von Ca2+-Homöostase und elektrischer Stabilität in der Transition zur Herzinsuffizienz führt"],["dc.relation.issn","1879-0844"],["dc.relation.workinggroup","RG El-Armouche"],["dc.relation.workinggroup","RG Hasenfuß (Transition zur Herzinsuffizienz)"],["dc.relation.workinggroup","RG L. Maier (Experimentelle Kardiologie)"],["dc.relation.workinggroup","RG Sossalla (Kardiovaskuläre experimentelle Elektrophysiologie und Bildgebung)"],["dc.relation.workinggroup","RG T. Fischer"],["dc.title","Activation of protein phosphatase 1 by a selective phosphatase disrupting peptide reduces sarcoplasmic reticulum Ca2+ leak in human heart failure"],["dc.type","journal_article"],["dc.type.internalPublication","unknown"],["dc.type.subtype","original_ja"],["dspace.entity.type","Publication"]]

[["dc.bibliographiccitation.firstpage","1728"],["dc.bibliographiccitation.issue","13"],["dc.bibliographiccitation.journal","Cardiovascular Research"],["dc.bibliographiccitation.lastpage","1737"],["dc.bibliographiccitation.volume","114"],["dc.contributor.author","Dybkova, Nataliya"],["dc.contributor.author","Ahmad, Shakil"],["dc.contributor.author","Pabel, Steffen"],["dc.contributor.author","Tirilomis, Petros"],["dc.contributor.author","Hartmann, Nico"],["dc.contributor.author","Fischer, Thomas H"],["dc.contributor.author","Bengel, Philipp"],["dc.contributor.author","Tirilomis, Theodoros"],["dc.contributor.author","Ljubojevic, Senka"],["dc.contributor.author","Renner, André"],["dc.contributor.author","Gummert, Jan"],["dc.contributor.author","Ellenberger, David"],["dc.contributor.author","Wagner, Stefan"],["dc.contributor.author","Frey, Norbert"],["dc.contributor.author","Maier, Lars S"],["dc.contributor.author","Streckfuss-Bömeke, Katrin"],["dc.contributor.author","Hasenfuss, Gerd"],["dc.contributor.author","Sossalla, Samuel"],["dc.date.accessioned","2020-12-10T18:18:48Z"],["dc.date.available","2020-12-10T18:18:48Z"],["dc.date.issued","2018"],["dc.identifier.doi","10.1093/cvr/cvy152"],["dc.identifier.pmid","29931291"],["dc.identifier.uri","https://resolver.sub.uni-goettingen.de/purl?gro-2/75097"],["dc.identifier.url","https://sfb1002.med.uni-goettingen.de/production/literature/publications/294"],["dc.language.iso","en"],["dc.notes.intern","DOI Import GROB-354"],["dc.relation","SFB 1002: Modulatorische Einheiten bei Herzinsuffizienz"],["dc.relation","SFB 1002 | A03: Bedeutung CaMKII-abhängiger Mechanismen für die Arrhythmogenese bei Herzinsuffizienz"],["dc.relation","SFB 1002 | A11: Absolute Arrhythmie bei Vorhofflimmern - ein neuer Mechanismus, der zu einer Störung von Ca2+-Homöostase und elektrischer Stabilität in der Transition zur Herzinsuffizienz führt"],["dc.relation","SFB 1002 | D01: Erholung aus der Herzinsuffizienz – Einfluss von Fibrose und Transkriptionssignatur"],["dc.relation.workinggroup","RG Hasenfuß (Transition zur Herzinsuffizienz)"],["dc.relation.workinggroup","RG L. Maier (Experimentelle Kardiologie)"],["dc.relation.workinggroup","RG Sossalla (Kardiovaskuläre experimentelle Elektrophysiologie und Bildgebung)"],["dc.relation.workinggroup","RG T. Fischer"],["dc.title","Differential regulation of sodium channels as a novel proarrhythmic mechanism in the human failing heart"],["dc.type","journal_article"],["dc.type.internalPublication","yes"],["dc.type.subtype","original_ja"],["dspace.entity.type","Publication"]]