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Wagner, Stefan
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Wagner, Stefan
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Wagner, Stefan
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Wagner, S.
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2018Journal Article [["dc.bibliographiccitation.firstpage","642"],["dc.bibliographiccitation.issue","4"],["dc.bibliographiccitation.journal","ESC Heart Failure"],["dc.bibliographiccitation.lastpage","648"],["dc.bibliographiccitation.volume","5"],["dc.contributor.author","Mustroph, Julian"],["dc.contributor.author","Wagemann, Olivia"],["dc.contributor.author","Lücht, Charlotte M."],["dc.contributor.author","Trum, Maximilian"],["dc.contributor.author","Hammer, Karin P."],["dc.contributor.author","Sag, Can Martin"],["dc.contributor.author","Lebek, Simon"],["dc.contributor.author","Tarnowski, Daniel"],["dc.contributor.author","Reinders, Jörg"],["dc.contributor.author","Perbellini, Filippo"],["dc.contributor.author","Terracciano, Cesare"],["dc.contributor.author","Schmid, Christof"],["dc.contributor.author","Schopka, Simon"],["dc.contributor.author","Hilker, Michael"],["dc.contributor.author","Zausig, York"],["dc.contributor.author","Pabel, Steffen"],["dc.contributor.author","Sossalla, Samuel T."],["dc.contributor.author","Schweda, Frank"],["dc.contributor.author","Maier, Lars S."],["dc.contributor.author","Wagner, Stefan"],["dc.date.accessioned","2020-12-10T14:06:09Z"],["dc.date.available","2020-12-10T14:06:09Z"],["dc.date.issued","2018"],["dc.identifier.doi","10.1002/ehf2.12336"],["dc.identifier.issn","2055-5822"],["dc.identifier.uri","https://resolver.sub.uni-goettingen.de/purl?gro-2/69797"],["dc.language.iso","en"],["dc.notes.intern","DOI Import GROB-354"],["dc.title","Empagliflozin reduces Ca/calmodulin-dependent kinase II activity in isolated ventricular cardiomyocytes"],["dc.title.alternative","Empagliflozin reduces CaMKII activity"],["dc.type","journal_article"],["dc.type.internalPublication","yes"],["dspace.entity.type","Publication"]]Details DOI2008Journal Article Research Paper [["dc.bibliographiccitation.firstpage","32"],["dc.bibliographiccitation.issue","1"],["dc.bibliographiccitation.journal","Journal of Molecular and Cellular Cardiology"],["dc.bibliographiccitation.lastpage","43"],["dc.bibliographiccitation.volume","45"],["dc.contributor.author","Sossalla, Samuel"],["dc.contributor.author","Wagner, Stefan"],["dc.contributor.author","Rasenack, Eva C. L."],["dc.contributor.author","Ruff, Hanna"],["dc.contributor.author","Weber, Sarah L."],["dc.contributor.author","Schoendube, Friedrich A."],["dc.contributor.author","Tirilomis, Theodor"],["dc.contributor.author","Tenderich, Gero"],["dc.contributor.author","Hasenfuß, Gerd"],["dc.contributor.author","Belardinelli, Luiz"],["dc.contributor.author","Maier, Lars S."],["dc.date.accessioned","2017-09-07T11:48:16Z"],["dc.date.available","2017-09-07T11:48:16Z"],["dc.date.issued","2008"],["dc.description.abstract","The goal of this study was to test the hypothesis that the novel anti-ischemic drug ratiolazine, which is known to inhibit late I-Na, could reduce intracellular [Na+](i) and diastolic [Ca2+](i) overload and improve diastolic function. Contractile dysfunction in human heart failure (HF) is associated with increased [Na+](i) and elevated diastolic [Ca2+](i). Increased Na influx through voltage-gated Na+ channels (late I-Na) has been suggested to contribute to elevated [Na+](i) in HF. In isometrically contracting ventricular muscle strips from end-stage failing human hearts, ranolazine (10 mu mol/L) did not exert negative inotropic effects on twitch force amplitude. However, ranolazine significantly reduced frequency-dependent increase in diastolic tension (i.e., diastolic dysfunction) by similar to 30% without significantly affecting sarcoplasmic reticulum (SR) Ca2+ loading. To investigate the mechanism of action of this beneficial effect of ranolazine on diastolic tension, Anemonia sulcata toxin II (ATX-II, 40 nmol/L) was used to increase intracellular Na+ loading in ventricular rabbit myocytes. ATX-II caused a significant rise in [Na+](i) typically seen in heart failure via increased late I-Na. In parallel, ATX-II significantly increased diastolic [Ca2+](i). In the presence of ranolazine the increases in late I-Na, as well as [Na+](i) and diastolic [Ca2+](i) were significantly blunted at all stimulation rates without significantly decreasing Ca2+ transient amplitudes or SR Ca2+ content. In summary, ranolazine reduced the frequency dependent increase in diastolic tension without having negative inotropic effects on contractility of muscles from end-stage failing human hearts. Moreover, in rabbit myocytes the increases in late I-Na, [Na+](i) and [Ca2+](i) caused by ATX-II, were significantly blunted by ranolazine. These results suggest that ratiolazine may be of therapeutic benefit in conditions of diastolic dysfunction due to elevated [Na+](i) and diastolic [Ca2+](i). (C) 2008 Elsevier Inc. All rights reserved."],["dc.identifier.doi","10.1016/j.yjmcc.2008.03.006"],["dc.identifier.gro","3143272"],["dc.identifier.isi","000257543800004"],["dc.identifier.pmid","18439620"],["dc.identifier.uri","https://resolver.sub.uni-goettingen.de/purl?gro-2/767"],["dc.notes.intern","WoS Import 2017-03-10"],["dc.notes.status","final"],["dc.notes.submitter","PUB_WoS_Import"],["dc.publisher","Academic Press Ltd- Elsevier Science Ltd"],["dc.relation.eissn","1095-8584"],["dc.relation.issn","0022-2828"],["dc.title","Ranolazine improves diastolic dysfunction in isolated myocardium from failing human hearts - Role of late sodium current and intracellular ion accumulation"],["dc.type","journal_article"],["dc.type.internalPublication","yes"],["dc.type.peerReviewed","yes"],["dc.type.subtype","original"],["dspace.entity.type","Publication"]]Details DOI PMID PMC WOS2006Journal Article Research Paper [["dc.bibliographiccitation.firstpage","1199"],["dc.bibliographiccitation.issue","7088"],["dc.bibliographiccitation.journal","Nature"],["dc.bibliographiccitation.lastpage","1203"],["dc.bibliographiccitation.volume","440"],["dc.contributor.author","Guan, Kaomei"],["dc.contributor.author","Nayernia, Karim"],["dc.contributor.author","Maier, Lars S."],["dc.contributor.author","Wagner, Stefan"],["dc.contributor.author","Dressel, Ralf"],["dc.contributor.author","Lee, Jae Ho"],["dc.contributor.author","Nolte, Jessica"],["dc.contributor.author","Wolf, F"],["dc.contributor.author","Li, M. Y."],["dc.contributor.author","Engel, Wolfgang"],["dc.contributor.author","Hasenfuß, Gerd"],["dc.date.accessioned","2017-09-07T11:53:07Z"],["dc.date.available","2017-09-07T11:53:07Z"],["dc.date.issued","2006"],["dc.description.abstract","Embryonic germ cells as well as germline stem cells from neonatal mouse testis are pluripotent and have differentiation potential similar to embryonic stem cells(1,2), suggesting that the germline lineage may retain the ability to generate pluripotent cells. However, until now there has been no evidence for the pluripotency and plasticity of adult spermatogonial stem cells (SSCs), which are responsible for maintaining spermatogenesis throughout life in the male(3). Here we show the isolation of SSCs from adult mouse testis using genetic selection, with a success rate of 27%. These isolated SSCs respond to culture conditions and acquire embryonic stem cell properties. We name these cells multipotent adult germline stem cells (maGSCs). They are able to spontaneously differentiate into derivatives of the three embryonic germ layers in vitro and generate teratomas in immunodeficient mice. When injected into an early blastocyst, SSCs contribute to the development of various organs and show germline transmission. Thus, the capacity to form multipotent cells persists in adult mouse testis. Establishment of human maGSCs from testicular biopsies may allow individual cell-based therapy without the ethical and immunological problems associated with human embryonic stem cells. Furthermore, these cells may provide new opportunities to study genetic diseases in various cell lineages."],["dc.identifier.doi","10.1038/nature04697"],["dc.identifier.gro","3143702"],["dc.identifier.isi","000237080000047"],["dc.identifier.pmid","16565704"],["dc.identifier.uri","https://resolver.sub.uni-goettingen.de/purl?gro-2/1245"],["dc.notes.intern","WoS Import 2017-03-10"],["dc.notes.status","final"],["dc.notes.submitter","PUB_WoS_Import"],["dc.relation.issn","0028-0836"],["dc.title","Pluripotency of spermatogonial stem cells from adult mouse testis"],["dc.type","journal_article"],["dc.type.internalPublication","yes"],["dc.type.peerReviewed","yes"],["dc.type.subtype","original"],["dspace.entity.type","Publication"]]Details DOI PMID PMC WOS2018Journal Article Research Paper [["dc.bibliographiccitation.firstpage","1690"],["dc.bibliographiccitation.issue","12"],["dc.bibliographiccitation.journal","European Journal of Heart Failure"],["dc.bibliographiccitation.lastpage","1700"],["dc.bibliographiccitation.volume","20"],["dc.contributor.author","Pabel, Steffen"],["dc.contributor.author","Wagner, Stefan"],["dc.contributor.author","Bollenberg, Hannah"],["dc.contributor.author","Bengel, Philipp"],["dc.contributor.author","Kovács, Árpád"],["dc.contributor.author","Schach, Christian"],["dc.contributor.author","Tirilomis, Petros"],["dc.contributor.author","Mustroph, Julian"],["dc.contributor.author","Renner, André"],["dc.contributor.author","Gummert, Jan"],["dc.contributor.author","Fischer, Thomas"],["dc.contributor.author","Van Linthout, Sophie"],["dc.contributor.author","Tschöpe, Carsten"],["dc.contributor.author","Streckfuss-Bömeke, Katrin"],["dc.contributor.author","Hasenfuss, Gerd"],["dc.contributor.author","Maier, Lars S."],["dc.contributor.author","Hamdani, Nazha"],["dc.contributor.author","Sossalla, Samuel"],["dc.date.accessioned","2019-02-19T13:12:22Z"],["dc.date.available","2019-02-19T13:12:22Z"],["dc.date.issued","2018"],["dc.description.abstract","Aims Empagliflozin, a clinically used oral antidiabetic drug that inhibits the sodium-dependent glucose co-transporter 2, has recently been evaluated for its cardiovascular safety. Surprisingly, empagliflozin reduced mortality and hospitalization for heart failure (HF) compared to placebo. However, the underlying mechanisms remain unclear. Therefore, our study aims to investigate whether empagliflozin may cause direct pleiotropic effects on the myocardium. Methods and results In order to assess possible direct myocardial effects of empagliflozin, we performed contractility experiments with in toto-isolated human systolic end-stage HF ventricular trabeculae. Empagliflozin significantly reduced diastolic tension, whereas systolic force was not changed. These results were confirmed in murine myocardium from diabetic and non-diabetic mice, suggesting independent effects from diabetic conditions. In human HF cardiomyocytes, empagliflozin did not influence calcium transient amplitude or diastolic calcium level. The mechanisms underlying the improved diastolic function were further elucidated by studying myocardial fibres from patients and rats with diastolic HF (HF with preserved ejection fraction, HFpEF). Empagliflozin beneficially reduced myofilament passive stiffness by enhancing phosphorylation levels of myofilament regulatory proteins. Intravenous injection of empagliflozin in anaesthetized HFpEF rats significantly improved diastolic function measured by echocardiography, while systolic contractility was unaffected. Conclusion Empagliflozin causes direct pleiotropic effects on the myocardium by improving diastolic stiffness and hence diastolic function. These effects were independent of diabetic conditions. Since pharmacological therapy of diastolic dysfunction and HF is an unmet need, our results provide a rationale for new translational studies and might also contribute to the understanding of the EMPA-REG OUTCOME trial."],["dc.identifier.doi","10.1002/ejhf.1328"],["dc.identifier.pmid","30328645"],["dc.identifier.uri","https://resolver.sub.uni-goettingen.de/purl?gro-2/57583"],["dc.identifier.url","https://sfb1002.med.uni-goettingen.de/production/literature/publications/239"],["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 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","Empagliflozin directly improves diastolic function in human heart failure"],["dc.type","journal_article"],["dc.type.internalPublication","unknown"],["dc.type.subtype","original_ja"],["dspace.entity.type","Publication"]]Details DOI PMID PMC2011Journal Article Research Paper [["dc.bibliographiccitation.firstpage","263"],["dc.bibliographiccitation.issue","2"],["dc.bibliographiccitation.journal","Basic Research in Cardiology"],["dc.bibliographiccitation.lastpage","272"],["dc.bibliographiccitation.volume","106"],["dc.contributor.author","Sossalla, Samuel"],["dc.contributor.author","Maurer, Ulrike"],["dc.contributor.author","Schotola, Hanna"],["dc.contributor.author","Hartmann, Nico H."],["dc.contributor.author","Didie, Michael"],["dc.contributor.author","Zimmermann, Wolfram-Hubertus"],["dc.contributor.author","Jacobshagen, Claudius"],["dc.contributor.author","Wagner, Stefan"],["dc.contributor.author","Maier, Lars S."],["dc.date.accessioned","2017-09-07T11:44:20Z"],["dc.date.available","2017-09-07T11:44:20Z"],["dc.date.issued","2011"],["dc.description.abstract","Transgenic (TG) Ca2+/calmodulin-dependent protein kinase II (CaMKII) delta(C) mice develop systolic heart failure (HF). CaMKII regulates intracellular Ca2+ handling proteins as well as sarcolemmal Na+ channels. We hypothesized that CaMKII also contributes to diastolic dysfunction and arrhythmias via augmentation of the late Na+ current (late I (Na)) in early HF (8-week-old TG mice). Echocardiography revealed severe diastolic dysfunction in addition to decreased systolic ejection fraction. Premature arrhythmogenic contractions (PACs) in isolated isometrically twitching papillary muscles only occurred in TG preparations (5 vs. 0, P < 0.05) which could be completely terminated when treated with the late I (Na) inhibitor ranolazine (Ran, 5 mu mol/L). Force-frequency relationships revealed significantly reduced twitch force amplitudes in TG papillary muscles. Most importantly, diastolic tension increased with raising frequencies to a greater extent in TG papillary muscles compared to WT specimen (at 10 Hz: 3.7 +/- A 0.4 vs. 2.5 +/- A 0.3 mN/mm(2); P < 0.05). Addition of Ran improved diastolic dysfunction to 2.1 +/- A 0.2 mN/mm(2) (at 10 Hz; P < 0.05) without negative inotropic effects. Mechanistically, the late I (Na) was markedly elevated in myocytes isolated from TG mice and could be completely reversed by Ran. In conclusion, our results show for the first time that TG CaMKII delta(C) overexpression induces diastolic dysfunction and arrhythmogenic triggers possibly via an enhanced late I (Na). Inhibition of elevated late I (Na) had beneficial effects on arrhythmias as well as diastolic function in papillary muscles from CaMKII delta(C) TG mice. Thus, late I (Na) inhibition appears to be a promising option for diastolic dysfunction and arrhythmias in HF where CaMKII is found to be increased."],["dc.identifier.doi","10.1007/s00395-010-0136-x"],["dc.identifier.gro","3142765"],["dc.identifier.isi","000286934300008"],["dc.identifier.pmid","21174213"],["dc.identifier.purl","https://resolver.sub.uni-goettingen.de/purl?gs-1/7315"],["dc.identifier.uri","https://resolver.sub.uni-goettingen.de/purl?gro-2/205"],["dc.notes.intern","WoS Import 2017-03-10"],["dc.notes.intern","Merged from goescholar"],["dc.notes.status","final"],["dc.notes.submitter","PUB_WoS_Import"],["dc.publisher","Springer"],["dc.publisher.place","Heidelberg"],["dc.relation.issn","0300-8428"],["dc.rights","Goescholar"],["dc.rights.uri","https://goescholar.uni-goettingen.de/licenses"],["dc.title","Diastolic dysfunction and arrhythmias caused by overexpression of CaMKII delta(C) can be reversed by inhibition of late Na+ current"],["dc.type","journal_article"],["dc.type.internalPublication","yes"],["dc.type.peerReviewed","yes"],["dc.type.subtype","original"],["dc.type.version","published_version"],["dspace.entity.type","Publication"]]Details DOI PMID PMC WOS2019Journal Article [["dc.bibliographiccitation.firstpage","726"],["dc.bibliographiccitation.issue","4"],["dc.bibliographiccitation.journal","Diabetologia"],["dc.bibliographiccitation.lastpage","729"],["dc.bibliographiccitation.volume","62"],["dc.contributor.author","Mustroph, Julian"],["dc.contributor.author","Lücht, Charlotte M."],["dc.contributor.author","Wagemann, Olivia"],["dc.contributor.author","Sowa, Thomas"],["dc.contributor.author","Hammer, Karin P."],["dc.contributor.author","Sag, Can M."],["dc.contributor.author","Tarnowski, Daniel"],["dc.contributor.author","Holzamer, Andreas"],["dc.contributor.author","Pabel, Steffen"],["dc.contributor.author","Beuthner, Bo Eric"],["dc.contributor.author","Sossalla, Samuel"],["dc.contributor.author","Maier, Lars S."],["dc.contributor.author","Wagner, Stefan"],["dc.date.accessioned","2019-07-09T11:51:32Z"],["dc.date.available","2019-07-09T11:51:32Z"],["dc.date.issued","2019"],["dc.identifier.doi","10.1007/s00125-019-4819-z"],["dc.identifier.pmid","30694352"],["dc.identifier.purl","https://resolver.sub.uni-goettingen.de/purl?gs-1/16145"],["dc.identifier.uri","https://resolver.sub.uni-goettingen.de/purl?gro-2/59964"],["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","Empagliflozin enhances human and murine cardiomyocyte glucose uptake by increased expression of GLUT1"],["dc.type","journal_article"],["dc.type.internalPublication","yes"],["dc.type.version","published_version"],["dspace.entity.type","Publication"]]Details DOI PMID PMC2020Journal Article [["dc.bibliographiccitation.journal","Frontiers in Cell and Developmental Biology"],["dc.bibliographiccitation.volume","8"],["dc.contributor.author","Li, Wener"],["dc.contributor.author","Stauske, Michael"],["dc.contributor.author","Luo, Xiaojing"],["dc.contributor.author","Wagner, Stefan"],["dc.contributor.author","Vollrath, Meike"],["dc.contributor.author","Mehnert, Carola S."],["dc.contributor.author","Schubert, Mario"],["dc.contributor.author","Cyganek, Lukas"],["dc.contributor.author","Chen, Simin"],["dc.contributor.author","Hasheminasab, Sayed-Mohammad"],["dc.contributor.author","Wulf, Gerald"],["dc.contributor.author","El-Armouche, Ali"],["dc.contributor.author","Maier, Lars S."],["dc.contributor.author","Hasenfuss, Gerd"],["dc.contributor.author","Guan, Kaomei"],["dc.date.accessioned","2021-04-14T08:31:12Z"],["dc.date.available","2021-04-14T08:31:12Z"],["dc.date.issued","2020"],["dc.identifier.doi","10.3389/fcell.2020.592893"],["dc.identifier.uri","https://resolver.sub.uni-goettingen.de/purl?gro-2/83516"],["dc.notes.intern","DOI Import GROB-399"],["dc.relation.eissn","2296-634X"],["dc.title","Disease Phenotypes and Mechanisms of iPSC-Derived Cardiomyocytes From Brugada Syndrome Patients With a Loss-of-Function SCN5A Mutation"],["dc.type","journal_article"],["dc.type.internalPublication","yes"],["dspace.entity.type","Publication"]]Details DOI2006Journal Article Research Paper [["dc.bibliographiccitation.firstpage","3127"],["dc.bibliographiccitation.issue","12"],["dc.bibliographiccitation.journal","Journal of Clinical Investigation"],["dc.bibliographiccitation.lastpage","3138"],["dc.bibliographiccitation.volume","116"],["dc.contributor.author","Wagner, Stefan"],["dc.contributor.author","Dybkova, Nataliya"],["dc.contributor.author","Rasenack, Eva C. L."],["dc.contributor.author","Jacobshagen, Claudius"],["dc.contributor.author","Fabritz, Larissa"],["dc.contributor.author","Kirchhof, Paulus"],["dc.contributor.author","Maier, Sebastian K. G."],["dc.contributor.author","Zhang, Tong"],["dc.contributor.author","Hasenfuß, Gerd"],["dc.contributor.author","Brown, Joan Heller"],["dc.contributor.author","Bers, Donald M."],["dc.contributor.author","Maier, Lars S."],["dc.date.accessioned","2017-09-07T11:49:54Z"],["dc.date.available","2017-09-07T11:49:54Z"],["dc.date.issued","2006"],["dc.description.abstract","In heart failure (HF), Ca2+/calmodulin kinase II (CaMKII) expression is increased. Altered Ne channel gating is linked to and may promote ventricular tachyarrhythmias (VTs) in HF. Calmodulin regulates Na+ channel gating, in part perhaps via CaMKII. We investigated effects of adenovirus-mediated (acute) and Tg (chronic) overexpression of cytosolic CaMKII delta(C) on Na+ current (IN) in rabbit and mouse ventricular myocytes, respectively (in whole-cell patch clamp). Both acute and chronic CaMKII delta(C) overexpression shifted voltage dependence of Na+ channel availability by -6 mV (P < 0.05), and the shift was Ca2+ dependent. CaMKII also enhanced intermediate inactivation and slowed recovery from inactivation (prevented by CaMKII inhibitors autocamtide 2-related inhibitory peptide [AIP] or KN93). CaMKII delta(C) markedly increased persistent (late) inward INa and intracellular Na+ concentration (as measured by the Na+ indicator sodium-binding benzofuran isophthalate [SBFI]), which was prevented by CaMKII inhibition in the case of acute CaMKII delta(C) overexpression. CaMKII coimmunoprecipitates with and phosphorylates Na+ channels. In vivo, transgenic CaMKII delta(C) overexpression prolonged QRS duration and repolarization (QT intervals), decreased effective refractory periods, and increased the propensity to develop VT. We conclude that CaMKII associates with and phosphorylates cardiac Na+ channels. This alters INa gating to reduce availability at high heart rate, while enhancing late INa (which could prolong action potential duration). In mice, enhanced CaMKII delta(C) activity predisposed to VT. Thus, CaMKII-dependent regulation of Na+ channel function may contribute to arrhythmogenesis in HF."],["dc.identifier.doi","10.1172/JCI26620"],["dc.identifier.gro","3143579"],["dc.identifier.isi","000242606900012"],["dc.identifier.pmid","17124532"],["dc.identifier.uri","https://resolver.sub.uni-goettingen.de/purl?gro-2/1108"],["dc.notes.intern","WoS Import 2017-03-10 / Funder: NHLBI NIH HHS [HL64724, HL80101, P01 HL080101, R01 HL064724]"],["dc.notes.status","final"],["dc.notes.submitter","PUB_WoS_Import"],["dc.publisher","Amer Soc Clinical Investigation Inc"],["dc.relation.issn","0021-9738"],["dc.title","Ca2+/calmodulin-dependent protein kinase II regulates cardiac Na+ channels"],["dc.type","journal_article"],["dc.type.internalPublication","yes"],["dc.type.peerReviewed","yes"],["dc.type.subtype","original"],["dspace.entity.type","Publication"]]Details DOI PMID PMC WOS2014Journal Article Overview [["dc.bibliographiccitation.artnumber","20"],["dc.bibliographiccitation.journal","Frontiers in Pharmacology"],["dc.bibliographiccitation.volume","5"],["dc.contributor.author","Mustroph, Julian"],["dc.contributor.author","Maier, Lars S."],["dc.contributor.author","Wagner, Stefan"],["dc.date.accessioned","2018-11-07T09:43:39Z"],["dc.date.available","2018-11-07T09:43:39Z"],["dc.date.issued","2014"],["dc.description.abstract","Cardiac K channels are critical determinants of cardiac excitability. In hypertrophied and failing myocardium, alterations in the expression and activity of voltage-gated K channels are frequently observed and contribute to the increased propensity for life-threatening arrhythmias. Thus, understanding the mechanisms of disturbed K channel regulation in heart failure (HF) is of critical importance. Amongst others, Ca/calmodulin-dependent protein kinase II (CaMKII) has been identified as an important regulator of K channel activity. In human HF but also various animal models, increased CaMKI I expression and activity has been linked to deteriorated contractile function and arrhythmias. This review will discuss the current knowledge about CaMKII regulation of several K channels, its influence on action potential properties, dispersion of repolanzation, and arrhythmias with special focus on HF"],["dc.description.sponsorship","Open-Access-Publikationsfonds 2014"],["dc.identifier.doi","10.3389/fphar.2014.00020"],["dc.identifier.isi","000347047500001"],["dc.identifier.pmid","24600393"],["dc.identifier.purl","https://resolver.sub.uni-goettingen.de/purl?gs-1/9943"],["dc.identifier.uri","https://resolver.sub.uni-goettingen.de/purl?gro-2/34226"],["dc.identifier.url","https://sfb1002.med.uni-goettingen.de/production/literature/publications/39"],["dc.language.iso","en"],["dc.notes.intern","Merged from goescholar"],["dc.notes.status","zu prüfen"],["dc.notes.submitter","Najko"],["dc.relation","SFB 1002: Modulatorische Einheiten bei Herzinsuffizienz"],["dc.relation","SFB 1002 | A03: Bedeutung CaMKII-abhängiger Mechanismen für die Arrhythmogenese bei Herzinsuffizienz"],["dc.relation.eissn","1663-9812"],["dc.relation.issn","1663-9812"],["dc.relation.workinggroup","RG L. Maier (Experimentelle Kardiologie)"],["dc.rights","CC BY 3.0"],["dc.rights.uri","https://creativecommons.org/licenses/by/3.0"],["dc.title","CaMKII regulation of cardiac K channels"],["dc.type","journal_article"],["dc.type.internalPublication","yes"],["dc.type.peerReviewed","yes"],["dc.type.subtype","overview_ja"],["dc.type.version","published_version"],["dspace.entity.type","Publication"]]Details DOI PMID PMC WOS2010Journal Article Research Paper [["dc.bibliographiccitation.firstpage","2330"],["dc.bibliographiccitation.issue","21"],["dc.bibliographiccitation.journal","Journal of the American College of Cardiology"],["dc.bibliographiccitation.lastpage","2342"],["dc.bibliographiccitation.volume","55"],["dc.contributor.author","Sossalla, Samuel"],["dc.contributor.author","Kallmeyer, Birte"],["dc.contributor.author","Wagner, Stefan"],["dc.contributor.author","Mazur, Marek"],["dc.contributor.author","Maurer, Ulrike"],["dc.contributor.author","Toischer, Karl"],["dc.contributor.author","Schmitto, Jan D."],["dc.contributor.author","Seipelt, Ralf"],["dc.contributor.author","Schoendube, Friedrich A."],["dc.contributor.author","Hasenfuß, Gerd"],["dc.contributor.author","Belardinelli, Luiz"],["dc.contributor.author","Maier, Lars S."],["dc.date.accessioned","2017-09-07T11:46:03Z"],["dc.date.available","2017-09-07T11:46:03Z"],["dc.date.issued","2010"],["dc.description.abstract","Objectives We investigated changes in Na+ currents (I-Na) in permanent (or chronic) atrial fibrillation (AF) and the effects of I-Na inhibition using ranolazine (Ran) on arrhythmias and contractility in human atrial myocardium. Background Electrical remodeling during AF is typically associated with alterations in Ca2+ and K+ currents. It remains unclear whether I-Na is also altered. Methods Right atrial appendages from patients with AF (n = 23) and in sinus rhythm (SR) (n = 79) were studied. Results Patch-clamp experiments in isolated atrial myocytes showed significantly reduced peak I-Na density (similar to 16%) in AF compared with SR, which was accompanied by a 26% lower expression of Nav1.5 (p < 0.05). In contrast, late I-Na was significantly increased in myocytes from AF atria by similar to 26%. Ran (10 mu mol/l) decreased late I-Na by similar to 60% (p < 0.05) in myocytes from patients with AF but only by similar to 18% (p < 0.05) in myocytes from SR atria. Proarrhythmic activity was elicited in atrial trabeculae exposed to high [Ca2+](o) or isoprenaline, which was significantly reversed by Ran (by 83% and 100%, respectively). Increasing pacing rates from 0.5 to 3.0 Hz led to an increase in diastolic tension that could be significantly decreased by Ran in atria from SR and AF patients. Conclusions Na+ channels may contribute to arrhythmias and contractile remodeling in AF. Inhibition of I-Na with Ran had antiarrhythmic effects and improved diastolic function. Thus, inhibition of late I-Na may be a promising new treatment option for patients with atrial rhythm disturbances and diastolic dysfunction. (J Am Coll Cardiol 2010;55:2330-42) (C) 2010 by the American College of Cardiology Foundation"],["dc.identifier.doi","10.1016/j.jacc.2009.12.055"],["dc.identifier.gro","3142922"],["dc.identifier.isi","000277805800007"],["dc.identifier.pmid","20488304"],["dc.identifier.purl","https://resolver.sub.uni-goettingen.de/purl?gs-1/6156"],["dc.identifier.uri","https://resolver.sub.uni-goettingen.de/purl?gro-2/379"],["dc.notes.intern","WoS Import 2017-03-10 / Funder: DFG [MA1982/4-1]; Klinische Forschergruppe [MA1982/2-2]; CV Therapeutics"],["dc.notes.intern","Merged from goescholar"],["dc.notes.status","final"],["dc.notes.submitter","PUB_WoS_Import"],["dc.publisher","Elsevier Science Inc"],["dc.relation.issn","0735-1097"],["dc.rights","Goescholar"],["dc.rights.uri","https://goescholar.uni-goettingen.de/licenses"],["dc.title","Altered Na+ Currents in Atrial Fibrillation Effects of Ranolazine on Arrhythmias and Contractility in Human Atrial Myocardium"],["dc.type","journal_article"],["dc.type.internalPublication","yes"],["dc.type.peerReviewed","yes"],["dc.type.subtype","original"],["dspace.entity.type","Publication"]]Details DOI PMID PMC WOS
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