Voigt, Niels

[["dc.bibliographiccitation.firstpage","82"],["dc.bibliographiccitation.issue","2"],["dc.bibliographiccitation.journal","Circulation"],["dc.bibliographiccitation.lastpage","92"],["dc.bibliographiccitation.volume","132"],["dc.contributor.author","Schmidt, Constanze"],["dc.contributor.author","Wiedmann, Felix"],["dc.contributor.author","Voigt, Niels"],["dc.contributor.author","Zhou, Xiao-Bo"],["dc.contributor.author","Heijman, Jordi"],["dc.contributor.author","Lang, Siegfried"],["dc.contributor.author","Albert, Virginia"],["dc.contributor.author","Kallenberger, Stefan"],["dc.contributor.author","Ruhparwar, Arjang"],["dc.contributor.author","Szabó, Gábor"],["dc.contributor.author","Thomas, Dierk"],["dc.date.accessioned","2022-03-01T11:43:54Z"],["dc.date.available","2022-03-01T11:43:54Z"],["dc.date.issued","2015"],["dc.description.abstract","Background— Antiarrhythmic management of atrial fibrillation (AF) remains a major clinical challenge. Mechanism-based approaches to AF therapy are sought to increase effectiveness and to provide individualized patient care. K 2P 3.1 (TASK-1 [tandem of P domains in a weak inward-rectifying K + channel–related acid-sensitive K + channel-1]) 2-pore-domain K + (K 2P ) channels have been implicated in action potential regulation in animal models. However, their role in the pathophysiology and treatment of paroxysmal and chronic patients with AF is unknown. Methods and Results— Right and left atrial tissue was obtained from patients with paroxysmal or chronic AF and from control subjects in sinus rhythm. Ion channel expression was analyzed by quantitative real-time polymerase chain reaction and Western blot. Membrane currents and action potentials were recorded using voltage- and current-clamp techniques. K 2P 3.1 subunits exhibited predominantly atrial expression, and atrial K 2P 3.1 transcript levels were highest among functional K 2P channels. K 2P 3.1 mRNA and protein levels were increased in chronic AF. Enhancement of corresponding currents in the right atrium resulted in shortened action potential duration at 90% of repolarization (APD 90 ) compared with patients in sinus rhythm. In contrast, K 2P 3.1 expression was not significantly affected in subjects with paroxysmal AF. Pharmacological K 2P 3.1 inhibition prolonged APD 90 in atrial myocytes from patients with chronic AF to values observed among control subjects in sinus rhythm. Conclusions— Enhancement of atrium-selective K 2P 3.1 currents contributes to APD shortening in patients with chronic AF, and K 2P 3.1 channel inhibition reverses AF-related APD shortening. These results highlight the potential of K 2P 3.1 as a novel drug target for mechanism-based AF therapy."],["dc.description.abstract","Background— Antiarrhythmic management of atrial fibrillation (AF) remains a major clinical challenge. Mechanism-based approaches to AF therapy are sought to increase effectiveness and to provide individualized patient care. K 2P 3.1 (TASK-1 [tandem of P domains in a weak inward-rectifying K + channel–related acid-sensitive K + channel-1]) 2-pore-domain K + (K 2P ) channels have been implicated in action potential regulation in animal models. However, their role in the pathophysiology and treatment of paroxysmal and chronic patients with AF is unknown. Methods and Results— Right and left atrial tissue was obtained from patients with paroxysmal or chronic AF and from control subjects in sinus rhythm. Ion channel expression was analyzed by quantitative real-time polymerase chain reaction and Western blot. Membrane currents and action potentials were recorded using voltage- and current-clamp techniques. K 2P 3.1 subunits exhibited predominantly atrial expression, and atrial K 2P 3.1 transcript levels were highest among functional K 2P channels. K 2P 3.1 mRNA and protein levels were increased in chronic AF. Enhancement of corresponding currents in the right atrium resulted in shortened action potential duration at 90% of repolarization (APD 90 ) compared with patients in sinus rhythm. In contrast, K 2P 3.1 expression was not significantly affected in subjects with paroxysmal AF. Pharmacological K 2P 3.1 inhibition prolonged APD 90 in atrial myocytes from patients with chronic AF to values observed among control subjects in sinus rhythm. Conclusions— Enhancement of atrium-selective K 2P 3.1 currents contributes to APD shortening in patients with chronic AF, and K 2P 3.1 channel inhibition reverses AF-related APD shortening. These results highlight the potential of K 2P 3.1 as a novel drug target for mechanism-based AF therapy."],["dc.identifier.doi","10.1161/CIRCULATIONAHA.114.012657"],["dc.identifier.uri","https://resolver.sub.uni-goettingen.de/purl?gro-2/102870"],["dc.language.iso","en"],["dc.notes.intern","DOI-Import GROB-531"],["dc.relation.eissn","1524-4539"],["dc.relation.issn","0009-7322"],["dc.title","Upregulation of K 2P 3.1 K + Current Causes Action Potential Shortening in Patients With Chronic Atrial Fibrillation"],["dc.type","journal_article"],["dc.type.internalPublication","unknown"],["dspace.entity.type","Publication"]]

[["dc.bibliographiccitation.issue","11"],["dc.bibliographiccitation.journal","Circulation"],["dc.bibliographiccitation.volume","133"],["dc.contributor.author","Schmidt, Constanze"],["dc.contributor.author","Wiedmann, Felix"],["dc.contributor.author","Voigt, Niels"],["dc.contributor.author","Zhou, Xiao-Bo"],["dc.contributor.author","Heijman, Jordi"],["dc.contributor.author","Lang, Siegfried"],["dc.contributor.author","Albert, Virginia"],["dc.contributor.author","Kallenberger, Stefan"],["dc.contributor.author","Ruhparwar, Arjang"],["dc.contributor.author","Szabó, Gábor"],["dc.contributor.author","Thomas, Dierk"],["dc.date.accessioned","2022-03-01T11:43:54Z"],["dc.date.available","2022-03-01T11:43:54Z"],["dc.date.issued","2016"],["dc.identifier.doi","10.1161/CIRCULATIONAHA.115.020662"],["dc.identifier.uri","https://resolver.sub.uni-goettingen.de/purl?gro-2/102872"],["dc.language.iso","en"],["dc.notes.intern","DOI-Import GROB-531"],["dc.relation.eissn","1524-4539"],["dc.relation.issn","0009-7322"],["dc.title","Response to Letter Regarding Article, “Upregulation of K 2P 3.1 K + Current Causes Action Potential Shortening in Patients With Chronic Atrial Fibrillation”"],["dc.type","journal_article"],["dc.type.internalPublication","unknown"],["dspace.entity.type","Publication"]]

[["dc.bibliographiccitation.firstpage","142"],["dc.bibliographiccitation.journal","Journal of Molecular and Cellular Cardiology"],["dc.bibliographiccitation.lastpage","152"],["dc.bibliographiccitation.volume","61"],["dc.contributor.author","Voigt, Niels"],["dc.contributor.author","Heijman, Jordi"],["dc.contributor.author","Trausch, Anne"],["dc.contributor.author","Mintert-Jancke, Elisa"],["dc.contributor.author","Pott, Lutz"],["dc.contributor.author","Ravens, Ursula"],["dc.contributor.author","Dobrev, Dobromir"],["dc.date.accessioned","2022-03-01T11:45:25Z"],["dc.date.available","2022-03-01T11:45:25Z"],["dc.date.issued","2013"],["dc.identifier.doi","10.1016/j.yjmcc.2013.03.011"],["dc.identifier.pii","S0022282813000928"],["dc.identifier.uri","https://resolver.sub.uni-goettingen.de/purl?gro-2/103319"],["dc.language.iso","en"],["dc.notes.intern","DOI-Import GROB-531"],["dc.relation.issn","0022-2828"],["dc.rights.uri","https://www.elsevier.com/tdm/userlicense/1.0/"],["dc.title","Impaired Na+-dependent regulation of acetylcholine-activated inward-rectifier K+ current modulates action potential rate dependence in patients with chronic atrial fibrillation"],["dc.type","journal_article"],["dc.type.internalPublication","unknown"],["dspace.entity.type","Publication"]]

[["dc.bibliographiccitation.firstpage","515"],["dc.bibliographiccitation.issue","6"],["dc.bibliographiccitation.journal","Journal of Cardiovascular Pharmacology"],["dc.bibliographiccitation.lastpage","522"],["dc.bibliographiccitation.volume","66"],["dc.contributor.author","Heijman, Jordi"],["dc.contributor.author","Voigt, Niels"],["dc.contributor.author","Ghezelbash, Shokoufeh"],["dc.contributor.author","Schirmer, Ilona"],["dc.contributor.author","Dobrev, Dobromir"],["dc.date.accessioned","2022-03-01T11:46:51Z"],["dc.date.available","2022-03-01T11:46:51Z"],["dc.date.issued","2015"],["dc.identifier.doi","10.1097/FJC.0000000000000253"],["dc.identifier.uri","https://resolver.sub.uni-goettingen.de/purl?gro-2/103823"],["dc.language.iso","en"],["dc.notes.intern","DOI-Import GROB-531"],["dc.relation.issn","0160-2446"],["dc.title","Calcium Handling Abnormalities as a Target for Atrial Fibrillation Therapeutics"],["dc.title.alternative","How Close to Clinical Implementation?"],["dc.type","journal_article"],["dc.type.internalPublication","unknown"],["dspace.entity.type","Publication"]]

[["dc.bibliographiccitation.firstpage","61"],["dc.bibliographiccitation.journal","International Journal of Cardiology"],["dc.bibliographiccitation.lastpage","68"],["dc.bibliographiccitation.volume","255"],["dc.contributor.author","Heijman, Jordi"],["dc.contributor.author","Kirchner, Dorit"],["dc.contributor.author","Kunze, Franziska"],["dc.contributor.author","Chrétien, Eva Maria"],["dc.contributor.author","Michel-Reher, Martina B."],["dc.contributor.author","Voigt, Niels"],["dc.contributor.author","Knaut, Michael"],["dc.contributor.author","Michel, Martin C."],["dc.contributor.author","Ravens, Ursula"],["dc.contributor.author","Dobrev, Dobromir"],["dc.date.accessioned","2022-03-01T11:45:10Z"],["dc.date.available","2022-03-01T11:45:10Z"],["dc.date.issued","2018"],["dc.identifier.doi","10.1016/j.ijcard.2017.12.050"],["dc.identifier.pii","S0167527317372625"],["dc.identifier.uri","https://resolver.sub.uni-goettingen.de/purl?gro-2/103235"],["dc.language.iso","en"],["dc.notes.intern","DOI-Import GROB-531"],["dc.relation.issn","0167-5273"],["dc.rights.uri","https://www.elsevier.com/tdm/userlicense/1.0/"],["dc.title","Muscarinic type-1 receptors contribute to I K,ACh in human atrial cardiomyocytes and are upregulated in patients with chronic atrial fibrillation"],["dc.type","journal_article"],["dc.type.internalPublication","unknown"],["dspace.entity.type","Publication"]]

[["dc.bibliographiccitation.firstpage","1764"],["dc.bibliographiccitation.issue","22"],["dc.bibliographiccitation.journal","European Heart Journal"],["dc.bibliographiccitation.lastpage","1774"],["dc.bibliographiccitation.volume","38"],["dc.contributor.author","Schmidt, Constanze"],["dc.contributor.author","Wiedmann, Felix"],["dc.contributor.author","Zhou, X."],["dc.contributor.author","Heijman, Jordi"],["dc.contributor.author","Voigt, Niels"],["dc.contributor.author","Ratte, Antonius"],["dc.contributor.author","Lang, Siegfried"],["dc.contributor.author","Kallenberger, Stefan M."],["dc.contributor.author","Campana, Chiara"],["dc.contributor.author","Weymann, Alexander"],["dc.contributor.author","De Simone, Raffaele"],["dc.contributor.author","Szabo, Gabor"],["dc.contributor.author","Ruhparwar, Arjang"],["dc.contributor.author","Kallenbach, Klaus"],["dc.contributor.author","Karck, Matthias"],["dc.contributor.author","Ehrlich, Joachim R."],["dc.contributor.author","Baczko, Istvan"],["dc.contributor.author","Borggrefe, Martin M."],["dc.contributor.author","Ravens, Ursula"],["dc.contributor.author","Dobrev, Dobromir"],["dc.contributor.author","Katus, Hugo A."],["dc.contributor.author","Thomas, Dierk"],["dc.date.accessioned","2018-11-07T10:22:47Z"],["dc.date.available","2018-11-07T10:22:47Z"],["dc.date.issued","2017"],["dc.description.abstract","Aims Atrial fibrillation (AF) prevalence increases with advanced stages of left ventricular (LV) dysfunction. Remote proarrhythmic effects of ventricular dysfunction on atrial electrophysiology remain incompletely understood. We hypothesized that repolarizing K(2P)3.1 K+ channels, previously implicated in AF pathophysiology, may contribute to shaping the atrial action potential (AP), forming a specific electrical substrate with LV dysfunction that might represent a target for personalized antiarrhythmic therapy. Methods and results A total of 175 patients exhibiting different stages of LV dysfunction were included. Ion channel expression was quantified by real-time polymerase chain reaction and Western blot. Membrane currents and APs were recorded from atrial cardiomyocytes using the patch-clamp technique. Severely reduced LV function was associated with decreased atrial K(2P)3.1 expression in sinus rhythm patients. In contrast, chronic (c) AF resulted in increased K(2P)3.1 levels, but paroxysmal (p) AF was not linked to significant K(2P)3.1 remodelling. LV dysfunction-related suppression of K(2P)3.1 currents prolonged atrial AP duration (APD) compared with patients with preserved LV function. In individuals with concomitant LV dysfunction and cAF, APD was determined by LV dysfunction-associated prolongation and by cAF-dependent shortening, respectively, consistent with changes in K(2P)3.1 abundance. K(2P)3.1 inhibition attenuated APD shortening in cAF patients irrespective of LV function, whereas in pAF subjects with severely reduced LV function, K(2P)3.1 blockade resulted in disproportionately high APD prolongation. Conclusion LV dysfunction is associated with reduction of atrial K(2P)3.1 channel expression, while cAF leads to increased K2P3.1 abundance. Differential remodelling of K(2P)3.1 and APD provides a basis for patient-tailored antiarrhythmic strategies."],["dc.identifier.doi","10.1093/eurheartj/ehw559"],["dc.identifier.isi","000402766900013"],["dc.identifier.pmid","28057773"],["dc.identifier.uri","https://resolver.sub.uni-goettingen.de/purl?gro-2/42338"],["dc.notes.status","zu prüfen"],["dc.notes.submitter","PUB_WoS_Import"],["dc.publisher","Oxford Univ Press"],["dc.relation.issn","1522-9645"],["dc.relation.issn","0195-668X"],["dc.title","Inverse remodelling of K(2P)3.1 K+ channel expression and action potential duration in left ventricular dysfunction and atrial fibrillation: implications for patient-specific antiarrhythmic drug therapy"],["dc.type","journal_article"],["dc.type.internalPublication","yes"],["dc.type.peerReviewed","yes"],["dc.type.status","published"],["dspace.entity.type","Publication"]]

[["dc.bibliographiccitation.journal","Frontiers in Pharmacology"],["dc.bibliographiccitation.volume","5"],["dc.contributor.author","Heijman, Jordi"],["dc.contributor.author","Voigt, Niels"],["dc.contributor.author","Wehrens, Xander H. T."],["dc.contributor.author","Dobrev, Dobromir"],["dc.date.accessioned","2022-03-01T11:44:23Z"],["dc.date.available","2022-03-01T11:44:23Z"],["dc.date.issued","2014"],["dc.identifier.doi","10.3389/fphar.2014.00030"],["dc.identifier.uri","https://resolver.sub.uni-goettingen.de/purl?gro-2/103014"],["dc.notes.intern","DOI-Import GROB-531"],["dc.relation.eissn","1663-9812"],["dc.title","Calcium dysregulation in atrial fibrillation: the role of CaMKII"],["dc.type","journal_article"],["dc.type.internalPublication","unknown"],["dspace.entity.type","Publication"]]

[["dc.bibliographiccitation.firstpage","77"],["dc.bibliographiccitation.lastpage","96"],["dc.contributor.author","Heijman, Jordi"],["dc.contributor.author","Molina, Cristina E."],["dc.contributor.author","Voigt, Niels"],["dc.contributor.editor","Thomas, Dierk"],["dc.contributor.editor","Remme, Carol Ann"],["dc.date.accessioned","2019-02-19T14:23:43Z"],["dc.date.available","2019-02-19T14:23:43Z"],["dc.date.issued","2018"],["dc.description.abstract","In cardiomyocytes voltage-gated Ca2+ channels are major players in cardiac cellular electrophysiology and cellular excitation-contraction coupling. Accordingly, Ca2+ channel dysfunction contributes to the development of cardiac arrhythmias and impaired cardiac contractile function. In addition, Ca2+ entry through voltage-gated Ca2+ channels is an important regulator of gene transcription and cardiac cellular metabolism. In order to fulfil these tasks reliably, Ca2+ channels are highly regulated by specific subunit compositions and various signaling pathways. This chapter provides an overview of the role of voltage-gated Ca2+ channels in cardiac cellular electrophysiology and summarizes their molecular composition, biophysical properties, and regulatory mechanisms, with a special focus on L-type Ca2+ channels."],["dc.identifier.doi","10.1007/978-3-319-77812-9_4"],["dc.identifier.uri","https://resolver.sub.uni-goettingen.de/purl?gro-2/57587"],["dc.identifier.url","https://sfb1002.med.uni-goettingen.de/production/literature/publications/233"],["dc.language.iso","en"],["dc.notes.status","final"],["dc.publisher","Springer"],["dc.publisher.place","Cham"],["dc.relation","SFB 1002: Modulatorische Einheiten bei Herzinsuffizienz"],["dc.relation","SFB 1002 | A13: Bedeutung einer gestörten zytosolischen Calciumpufferung bei der atrialen Arrhythmogenese bei Patienten mit Herzinsuffizienz (HF)"],["dc.relation.crisseries","Cardiac and Vascular Biology"],["dc.relation.isbn","978-3-319-77811-2"],["dc.relation.isbn","978-3-319-77812-9"],["dc.relation.ispartof","Channelopathies in Heart Disease"],["dc.relation.ispartofseries","Cardiac and Vascular Biology"],["dc.relation.issn","2509-7830"],["dc.relation.issn","2509-7849"],["dc.relation.workinggroup","RG Voigt (Molecular Pharmacology)"],["dc.title","Voltage-Gated Calcium Channels and Their Roles in Cardiac Electrophysiology"],["dc.type","book_chapter"],["dc.type.internalPublication","unknown"],["dspace.entity.type","Publication"]]

[["dc.bibliographiccitation.firstpage","881"],["dc.bibliographiccitation.issue","9"],["dc.bibliographiccitation.journal","Circulation"],["dc.bibliographiccitation.lastpage","897"],["dc.bibliographiccitation.volume","135"],["dc.contributor.author","Abu-Taha, Issam H."],["dc.contributor.author","Heijman, Jordi"],["dc.contributor.author","Hippe, Hans-Jörg"],["dc.contributor.author","Wolf, Nadine M."],["dc.contributor.author","El-Armouche, Ali"],["dc.contributor.author","Nikolaev, Viacheslav O."],["dc.contributor.author","Schäfer, Marina"],["dc.contributor.author","Würtz, Christina M."],["dc.contributor.author","Neef, Stefan"],["dc.contributor.author","Voigt, Niels"],["dc.contributor.author","Baczkó, István"],["dc.contributor.author","Varró, András"],["dc.contributor.author","Müller, Marion"],["dc.contributor.author","Meder, Benjamin"],["dc.contributor.author","Katus, Hugo A."],["dc.contributor.author","Spiger, Katharina"],["dc.contributor.author","Vettel, Christiane"],["dc.contributor.author","Lehmann, Lorenz H."],["dc.contributor.author","Backs, Johannes"],["dc.contributor.author","Skolnik, Edward Y."],["dc.contributor.author","Lutz, Susanne"],["dc.contributor.author","Dobrev, Dobromir"],["dc.contributor.author","Wieland, Thomas"],["dc.date.accessioned","2020-12-10T18:38:01Z"],["dc.date.available","2020-12-10T18:38:01Z"],["dc.date.issued","2017"],["dc.description.abstract","Background: Chronic heart failure (HF) is associated with altered signal transduction via -adrenoceptors and G proteins and with reduced cAMP formation. Nucleoside diphosphate kinases (NDPKs) are enriched at the plasma membrane of patients with end-stage HF, but the functional consequences of this are largely unknown, particularly for NDPK-C. Here, we investigated the potential role of NDPK-C in cardiac cAMP formation and contractility. Methods: Real-time polymerase chain reaction, (far) Western blot, immunoprecipitation, and immunocytochemistry were used to study the expression, interaction with G proteins, and localization of NDPKs. cAMP levels were determined with immunoassays or fluorescent resonance energy transfer, and contractility was determined in cardiomyocytes (cell shortening) and in vivo (fractional shortening). Results: NDPK-C was essential for the formation of an NDPK-B/G protein complex. Protein and mRNA levels of NDPK-C were upregulated in end-stage human HF, in rats after long-term isoprenaline stimulation through osmotic minipumps, and after incubation of rat neonatal cardiomyocytes with isoprenaline. Isoprenaline also promoted translocation of NDPK-C to the plasma membrane. Overexpression of NDPK-C in cardiomyocytes increased cAMP levels and sensitized cardiomyocytes to isoprenaline-induced augmentation of contractility, whereas NDPK-C knockdown decreased cAMP levels. In vivo, depletion of NDPK-C in zebrafish embryos caused cardiac edema and ventricular dysfunction. NDPK-B knockout mice had unaltered NDPK-C expression but showed contractile dysfunction and exacerbated cardiac remodeling during long-term isoprenaline stimulation. In human end-stage HF, the complex formation between NDPK-C and G(i2) was increased whereas the NDPK-C/G(s) interaction was decreased, producing a switch that may contribute to an NDPK-C-dependent cAMP reduction in HF. Conclusions: Our findings identify NDPK-C as an essential requirement for both the interaction between NDPK isoforms and between NDPK isoforms and G proteins. NDPK-C is a novel critical regulator of -adrenoceptor/cAMP signaling and cardiac contractility. By switching from G(s) to G(i2) activation, NDPK-C may contribute to lower cAMP levels and the related contractile dysfunction in HF."],["dc.identifier.doi","10.1161/CIRCULATIONAHA.116.022852"],["dc.identifier.eissn","1524-4539"],["dc.identifier.isi","000395549700016"],["dc.identifier.issn","0009-7322"],["dc.identifier.pmid","27927712"],["dc.identifier.uri","https://resolver.sub.uni-goettingen.de/purl?gro-2/77166"],["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","1524-4539"],["dc.relation.issn","0009-7322"],["dc.title","Nucleoside Diphosphate Kinase-C Suppresses cAMP Formation in Human Heart Failure"],["dc.type","journal_article"],["dc.type.internalPublication","yes"],["dc.type.peerReviewed","yes"],["dc.type.status","published"],["dspace.entity.type","Publication"]]

[["dc.bibliographiccitation.firstpage","537"],["dc.bibliographiccitation.issue","3"],["dc.bibliographiccitation.journal","The Journal of Physiology"],["dc.bibliographiccitation.lastpage","553"],["dc.bibliographiccitation.volume","594"],["dc.contributor.author","Heijman, Jordi"],["dc.contributor.author","Erfanian Abdoust, Pegah"],["dc.contributor.author","Voigt, Niels"],["dc.contributor.author","Nattel, Stanley"],["dc.contributor.author","Dobrev, Dobromir"],["dc.date.accessioned","2022-03-01T11:47:11Z"],["dc.date.available","2022-03-01T11:47:11Z"],["dc.date.issued","2015"],["dc.identifier.doi","10.1113/JP271404"],["dc.identifier.uri","https://resolver.sub.uni-goettingen.de/purl?gro-2/103941"],["dc.language.iso","en"],["dc.notes.intern","DOI-Import GROB-531"],["dc.relation.issn","0022-3751"],["dc.title","Computational models of atrial cellular electrophysiology and calcium handling, and their role in atrial fibrillation"],["dc.title.alternative","Computational modelling of atrial Ca\r\n 2+\r\n handling"],["dc.type","journal_article"],["dc.type.internalPublication","unknown"],["dspace.entity.type","Publication"]]