Voigt, Niels

[["dc.bibliographiccitation.firstpage","1119"],["dc.bibliographiccitation.issue","7"],["dc.bibliographiccitation.journal","Europace"],["dc.bibliographiccitation.lastpage","1131"],["dc.bibliographiccitation.volume","22"],["dc.contributor.author","Hofhuis, Julia"],["dc.contributor.author","Bersch, Kristina"],["dc.contributor.author","Wagner, Stefan"],["dc.contributor.author","Molina, Cristina Espinosa"],["dc.contributor.author","Fakuade, Funsho E."],["dc.contributor.author","Iyer, Lavanya M."],["dc.contributor.author","Streckfuß-Bömeke, Katrin"],["dc.contributor.author","Toischer, Karl"],["dc.contributor.author","Zelarayan, Laura Cecilia"],["dc.contributor.author","Voigt, Niels"],["dc.contributor.author","Nikolaev, Viacheslav O."],["dc.contributor.author","Maier, Lars Siegfried"],["dc.contributor.author","Klinge, Lars"],["dc.contributor.author","Thoms, Sven"],["dc.date.accessioned","2020-08-10T05:34:04Z"],["dc.date.available","2020-08-10T05:34:04Z"],["dc.date.issued","2020"],["dc.description.abstract","The multi-C2 domain protein dysferlin localizes to the T-Tubule system of skeletal and heart muscles. In skeletal muscle, dysferlin is known to play a role in membrane repair and in T-tubule biogenesis and maintenance. Dysferlin deficiency manifests as muscular dystrophy of proximal and distal muscles. Cardiomyopathies have been also reported, and some dysferlinopathy mouse models develop cardiac dysfunction under stress. Generally, the role and functional relevance of dysferlin in the heart is not clear. The aim of this study was to analyse the effect of dysferlin deficiency on the transverse-axial tubule system (TATS) structure and on Ca2+ homeostasis in the heart."],["dc.identifier.doi","10.1093/europace/euaa093"],["dc.identifier.pmid","32572487"],["dc.identifier.uri","https://resolver.sub.uni-goettingen.de/purl?gro-2/67547"],["dc.identifier.url","https://sfb1002.med.uni-goettingen.de/production/literature/publications/360"],["dc.language.iso","en"],["dc.relation","SFB 1002: Modulatorische Einheiten bei Herzinsuffizienz"],["dc.relation","SFB 1002 | A10: Peroxisomen als modulatorische Einheiten im Herzstoffwechsel und bei Herzinsuffizienz"],["dc.relation","SFB 1002 | C07: Kardiomyozyten Wnt/β-catenin Komplex Aktivität im pathologischen Herz-Remodeling - als gewebespezifischer therapeutischer Ansatz"],["dc.relation","SFB 1002 | D04: Bedeutung der Methylierung von RNA (m6A) und des Histons H3 (H3K4) in der Herzinsuffizienz"],["dc.relation","SFB 1002 | S01: In vivo und in vitro Krankheitsmodelle"],["dc.relation","SFB 1002 | A13: Bedeutung einer gestörten zytosolischen Calciumpufferung bei der atrialen Arrhythmogenese bei Patienten mit Herzinsuffizienz (HF)"],["dc.relation.eissn","1532-2092"],["dc.relation.issn","1099-5129"],["dc.relation.workinggroup","RG L. Maier (Experimentelle Kardiologie)"],["dc.relation.workinggroup","RG Nikolaev (Cardiovascular Research Center)"],["dc.relation.workinggroup","RG Thoms (Biochemistry and Molecular Medicine)"],["dc.relation.workinggroup","RG Toischer (Kardiales Remodeling)"],["dc.relation.workinggroup","RG Voigt (Molecular Pharmacology)"],["dc.relation.workinggroup","RG Zelarayán-Behrend (Developmental Pharmacology)"],["dc.title","Dysferlin links excitation-contraction coupling to structure and maintenance of the cardiac transverse-axial tubule system"],["dc.type","journal_article"],["dc.type.internalPublication","yes"],["dc.type.subtype","original_ja"],["dspace.entity.type","Publication"]]

[["dc.bibliographiccitation.firstpage","5"],["dc.bibliographiccitation.issue","1"],["dc.bibliographiccitation.journal","Basic Research in Cardiology"],["dc.bibliographiccitation.volume","117"],["dc.contributor.author","Jung, Philipp"],["dc.contributor.author","Seibertz, Fitzwilliam"],["dc.contributor.author","Fakuade, Funsho E."],["dc.contributor.author","Ignatyeva, Nadezda"],["dc.contributor.author","Sampathkumar, Shrivatsan"],["dc.contributor.author","Ritter, Melanie"],["dc.contributor.author","Li, Housen"],["dc.contributor.author","Mason, Fleur E."],["dc.contributor.author","Ebert, Antje"],["dc.contributor.author","Voigt, Niels"],["dc.date.accessioned","2022-05-24T06:53:38Z"],["dc.date.available","2022-05-24T06:53:38Z"],["dc.date.issued","2022-05-02"],["dc.description.abstract","Dilated cardiomyopathy (DCM) is a major risk factor for heart failure and is associated with the development of life-threatening cardiac arrhythmias. Using a patient-specific induced pluripotent stem cell-derived cardiomyocyte (iPSC-CM) model harbouring a mutation in cardiac troponin T (R173W), we aim to examine the cellular basis of arrhythmogenesis in DCM patients with this mutation. iPSC from control (Ctrl) and DCM-TnT-R173W donors from the same family were differentiated into iPSC-CM and analysed through optical action potential (AP) recordings, simultaneous measurement of cytosolic calcium concentration ([Ca2+]i) and membrane currents and separately assayed using field stimulation to detect the threshold for AP- and [Ca2+]i-alternans development. AP duration was unaltered in TnT-R173W iPSC-CM. Nevertheless, TnT-R173W iPSC-CM showed a strikingly low stimulation threshold for AP- and [Ca2+]i-alternans. Myofilaments are known to play a role as intracellular Ca2+ buffers and here we show increased Ca2+ affinity of intracellular buffers in TnT-R173W cells, indicating increased myofilament sensitivity to Ca2+. Similarly, EMD57033, a myofilament Ca2+ sensitiser, replicated the abnormal [Ca2+]i dynamics observed in TnT-R173W samples and lowered the threshold for alternans development. In contrast, application of a Ca2+ desensitiser (blebbistatin) to TnT-R173W iPSC-CM was able to phenotypically rescue Ca2+ dynamics, normalising Ca2+ transient profile and minimising the occurrence of Ca2+ alternans at physiological frequencies. This finding suggests that increased Ca2+ buffering likely plays a major arrhythmogenic role in patients with DCM, specifically in those with mutations in cardiac troponin T. In addition, we propose that modulation of myofilament Ca2+ sensitivity could be an effective anti-arrhythmic target for pharmacological management of this disease."],["dc.identifier.doi","10.1007/s00395-022-00912-z"],["dc.identifier.pmid","35499658"],["dc.identifier.uri","https://resolver.sub.uni-goettingen.de/purl?gro-2/108251"],["dc.identifier.url","https://sfb1002.med.uni-goettingen.de/production/literature/publications/430"],["dc.identifier.url","https://mbexc.uni-goettingen.de/literature/publications/482"],["dc.language.iso","en"],["dc.relation","SFB 1002: Modulatorische Einheiten bei Herzinsuffizienz"],["dc.relation","EXC 2067: Multiscale Bioimaging"],["dc.relation.eissn","1435-1803"],["dc.relation.issn","0300-8428"],["dc.relation.workinggroup","RG Ebert (Cardiovascular Cell Biology and Systems Medicine)"],["dc.relation.workinggroup","RG Voigt (Molecular Pharmacology)"],["dc.rights","CC BY 4.0"],["dc.title","Increased cytosolic calcium buffering contributes to a cellular arrhythmogenic substrate in iPSC-cardiomyocytes from patients with dilated cardiomyopathy"],["dc.type","journal_article"],["dc.type.internalPublication","yes"],["dc.type.subtype","original_ja"],["dc.type.version","published_version"],["dspace.entity.type","Publication"]]

[["dc.bibliographiccitation.artnumber","1227"],["dc.bibliographiccitation.journal","Frontiers in Physiology"],["dc.bibliographiccitation.volume","9"],["dc.contributor.author","Brandenburg, Sören"],["dc.contributor.author","Pawlowitz, Jan"],["dc.contributor.author","Lehnart, Stephan Elmar"],["dc.contributor.author","Fakuade, Funsho E."],["dc.contributor.author","Kownatzki-Danger, Daniel"],["dc.contributor.author","Kohl, Tobias"],["dc.contributor.author","Mitronova, Gyuzel Y."],["dc.contributor.author","Scardigli, Marina"],["dc.contributor.author","Neef, Jakob"],["dc.contributor.author","Schmidt, Constanze"],["dc.contributor.author","Wiedmann, Felix"],["dc.contributor.author","Pavone, Francesco S."],["dc.contributor.author","Sacconi, Leonardo"],["dc.contributor.author","Kutschka, Ingo"],["dc.contributor.author","Sossalla, Samuel"],["dc.contributor.author","Moser, Tobias"],["dc.contributor.author","Voigt, Niels"],["dc.date.accessioned","2022-05-13T09:20:22Z"],["dc.date.available","2022-05-13T09:20:22Z"],["dc.date.issued","2018-07-13"],["dc.description.abstract","Rationale: Recently, abundant axial tubule (AT) membrane structures were identified deep inside atrial myocytes (AMs). Upon excitation, ATs rapidly activate intracellular Ca2+ release and sarcomeric contraction through extensive AT junctions, a cell-specific atrial mechanism. While AT junctions with the sarcoplasmic reticulum contain unusually large clusters of ryanodine receptor 2 (RyR2) Ca2+ release channels in mouse AMs, it remains unclear if similar protein networks and membrane structures exist across species, particularly those relevant for atrial disease modeling. Objective: To examine and quantitatively analyze the architecture of AT membrane structures and associated Ca2+ signaling proteins across species from mouse to human. Methods and Results: We developed superresolution microscopy (nanoscopy) strategies for intact live AMs based on a new custom-made photostable cholesterol dye and immunofluorescence imaging of membraneous structures and membrane proteins in fixed tissue sections from human, porcine, and rodent atria. Consistently, in mouse, rat, and rabbit AMs, intact cell-wide tubule networks continuous with the surface membrane were observed, mainly composed of ATs. Moreover, co-immunofluorescence nanoscopy showed L-type Ca2+ channel clusters adjacent to extensive junctional RyR2 clusters at ATs. However, only junctional RyR2 clusters were highly phosphorylated and may thus prime Ca2+ release at ATs, locally for rapid signal amplification. While the density of the integrated L-type Ca2+ current was similar in human and mouse AMs, the intracellular Ca2+ transient showed quantitative differences. Importantly, local intracellular Ca2+ release from AT junctions occurred through instantaneous action potential propagation via transverse tubules (TTs) from the surface membrane. Hence, sparse TTs were sufficient as electrical conduits for rapid activation of Ca2+ release through ATs. Nanoscopy of atrial tissue sections confirmed abundant ATs as the major network component of AMs, particularly in human atrial tissue sections. Conclusion: AT junctions represent a conserved, cell-specific membrane structure for rapid excitation-contraction coupling throughout a representative spectrum of species including human. Since ATs provide the major excitable membrane network component in AMs, a new model of atrial \"super-hub\" Ca2+ signaling may apply across biomedically relevant species, opening avenues for future investigations about atrial disease mechanisms and therapeutic targeting."],["dc.identifier.doi","10.3389/fphys.2018.01227"],["dc.identifier.pmid","30349482"],["dc.identifier.purl","https://resolver.sub.uni-goettingen.de/purl?gs-1/15400"],["dc.identifier.uri","https://resolver.sub.uni-goettingen.de/purl?gro-2/107860"],["dc.identifier.url","https://sfb1002.med.uni-goettingen.de/production/literature/publications/217"],["dc.language.iso","en"],["dc.notes.intern","Merged from goescholar"],["dc.relation","SFB 1002: Modulatorische Einheiten bei Herzinsuffizienz"],["dc.relation","SFB 1002 | A05: Molekulares Imaging von kardialen Calcium-Freisetzungsdomänen"],["dc.relation","SFB 1002 | A09: Lokale molekulare Nanodomänen-Regulation der kardialen Ryanodin-Rezeptor-Funktion"],["dc.relation","SFB 1002 | S02: Hochauflösende Fluoreszenzmikroskopie und integrative Datenanalyse"],["dc.relation","SFB 1002 | A13: Bedeutung einer gestörten zytosolischen Calciumpufferung bei der atrialen Arrhythmogenese bei Patienten mit Herzinsuffizienz (HF)"],["dc.relation.eissn","1664-042X"],["dc.relation.workinggroup","RG Brandenburg"],["dc.relation.workinggroup","RG Lehnart (Cellular Biophysics and Translational Cardiology Section)"],["dc.relation.workinggroup","RG Sossalla (Kardiovaskuläre experimentelle Elektrophysiologie und Bildgebung)"],["dc.relation.workinggroup","RG Voigt (Molecular Pharmacology)"],["dc.rights","CC BY 4.0"],["dc.rights.uri","https://creativecommons.org/licenses/by/4.0"],["dc.subject.ddc","610"],["dc.title","Axial Tubule Junctions Activate Atrial Ca2+ Release across Species"],["dc.type","research_data"],["dc.type.internalPublication","yes"],["dc.type.subtype","original_ja"],["dc.type.version","published_version"],["dspace.entity.type","Publication"]]

[["dc.bibliographiccitation.issue","1"],["dc.bibliographiccitation.journal","Communications Biology"],["dc.bibliographiccitation.volume","5"],["dc.contributor.author","Seibertz, Fitzwilliam"],["dc.contributor.author","Rapedius, Markus"],["dc.contributor.author","Fakuade, Funsho E."],["dc.contributor.author","Tomsits, Philipp"],["dc.contributor.author","Liutkute, Aiste"],["dc.contributor.author","Cyganek, Lukas"],["dc.contributor.author","Becker, Nadine"],["dc.contributor.author","Majumder, Rupamanjari"],["dc.contributor.author","Clauß, Sebastian"],["dc.contributor.author","Fertig, Niels"],["dc.contributor.author","Voigt, Niels"],["dc.date.accessioned","2022-10-04T10:21:07Z"],["dc.date.available","2022-10-04T10:21:07Z"],["dc.date.issued","2022"],["dc.description.abstract","Abstract\n Crucial conventional patch-clamp approaches to investigate cellular electrophysiology suffer from low-throughput and require considerable experimenter expertise. Automated patch-clamp (APC) approaches are more experimenter independent and offer high-throughput, but by design are predominantly limited to assays containing small, homogenous cells. In order to enable high-throughput APC assays on larger cells such as native cardiomyocytes isolated from mammalian hearts, we employed a fixed-well APC plate format. A broad range of detailed electrophysiological parameters including action potential, L-type calcium current and basal inward rectifier current were reliably acquired from isolated swine atrial and ventricular cardiomyocytes using APC. Effective pharmacological modulation also indicated that this technique is applicable for drug screening using native cardiomyocyte material. Furthermore, sequential acquisition of multiple parameters from a single cell was successful in a high throughput format, substantially increasing data richness and quantity per experimental run. When appropriately expanded, these protocols will provide a foundation for effective mechanistic and phenotyping studies of human cardiac electrophysiology. Utilizing scarce biopsy samples, regular high throughput characterization of primary cardiomyocytes using APC will facilitate drug development initiatives and personalized treatment strategies for a multitude of cardiac diseases."],["dc.description.sponsorship"," Deutsche Forschungsgemeinschaft https://doi.org/10.13039/501100001659"],["dc.description.sponsorship"," Deutsches Zentrum für Herz-Kreislaufforschung https://doi.org/10.13039/100010447"],["dc.identifier.doi","10.1038/s42003-022-03871-2"],["dc.identifier.pii","3871"],["dc.identifier.uri","https://resolver.sub.uni-goettingen.de/purl?gro-2/114333"],["dc.language.iso","en"],["dc.notes.intern","DOI-Import GROB-600"],["dc.relation.eissn","2399-3642"],["dc.rights.uri","https://creativecommons.org/licenses/by/4.0"],["dc.title","A modern automated patch-clamp approach for high throughput electrophysiology recordings in native cardiomyocytes"],["dc.type","journal_article"],["dc.type.internalPublication","yes"],["dspace.entity.type","Publication"]]

[["dc.bibliographiccitation.firstpage","2545"],["dc.bibliographiccitation.issue","11"],["dc.bibliographiccitation.journal","The Journal of Physiology"],["dc.bibliographiccitation.lastpage","2546"],["dc.bibliographiccitation.volume","600"],["dc.contributor.affiliation","Fakuade, Funsho E.; 1\r\nInstitute of Pharmacology and Toxicology\r\nUniversity Medical Center Göttingen\r\nGermany"],["dc.contributor.affiliation","Fauconnier, Jeremy; 3\r\nPhyMedExp, INSERM, CNRS\r\nUniversité de Montpellier\r\nMontpellier France"],["dc.contributor.author","Fakuade, Funsho E."],["dc.contributor.author","Fauconnier, Jeremy"],["dc.contributor.author","Voigt, Niels"],["dc.date.accessioned","2022-05-02T08:02:30Z"],["dc.date.available","2022-05-02T08:02:30Z"],["dc.date.issued","2022"],["dc.date.updated","2022-11-11T13:13:50Z"],["dc.description.sponsorship","Fondation de France http://dx.doi.org/10.13039/501100004431"],["dc.description.sponsorship","French National Research Agency http://dx.doi.org/10.13039/501100001665"],["dc.description.sponsorship","German Research Foundation http://dx.doi.org/10.13039/501100001659"],["dc.description.sponsorship","German Research Foundation under Germany's Excellence Strategy"],["dc.description.sponsorship","German Centre for Cardiovascular Research http://dx.doi.org/10.13039/100010447"],["dc.identifier.doi","10.1113/JP283032"],["dc.identifier.pmid","35451079"],["dc.identifier.uri","https://resolver.sub.uni-goettingen.de/purl?gro-2/107342"],["dc.identifier.url","https://mbexc.uni-goettingen.de/literature/publications/495"],["dc.identifier.url","https://sfb1002.med.uni-goettingen.de/production/literature/publications/434"],["dc.language.iso","en"],["dc.notes.intern","DOI Import GROB-561"],["dc.relation","EXC 2067: Multiscale Bioimaging"],["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.eissn","1469-7793"],["dc.relation.issn","0022-3751"],["dc.relation.workinggroup","RG Voigt (Molecular Pharmacology)"],["dc.rights","CC BY 4.0"],["dc.rights.uri","http://onlinelibrary.wiley.com/termsAndConditions#vor"],["dc.title","Background calcium influx in arrhythmia: lead actor or extra?"],["dc.type","journal_article"],["dc.type.internalPublication","yes"],["dc.type.subtype","original_ja"],["dc.type.version","published_version"],["dspace.entity.type","Publication"]]

[["dc.bibliographiccitation.firstpage","4"],["dc.bibliographiccitation.issue","1"],["dc.bibliographiccitation.journal","Cardiovascular Research"],["dc.bibliographiccitation.lastpage","6"],["dc.bibliographiccitation.volume","117"],["dc.contributor.author","Fakuade, Funsho E."],["dc.contributor.author","Tomsits, Philipp"],["dc.contributor.author","Voigt, Niels"],["dc.date.accessioned","2021-04-14T08:30:10Z"],["dc.date.available","2021-04-14T08:30:10Z"],["dc.date.issued","2020"],["dc.identifier.doi","10.1093/cvr/cvaa308"],["dc.identifier.pmid","33112373"],["dc.identifier.uri","https://resolver.sub.uni-goettingen.de/purl?gro-2/83131"],["dc.identifier.url","https://mbexc.uni-goettingen.de/literature/publications/147"],["dc.identifier.url","https://sfb1002.med.uni-goettingen.de/production/literature/publications/385"],["dc.language.iso","en"],["dc.notes.intern","DOI Import GROB-399"],["dc.relation","EXC 2067: Multiscale Bioimaging"],["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.eissn","1755-3245"],["dc.relation.issn","0008-6363"],["dc.relation.workinggroup","RG Voigt (Molecular Pharmacology)"],["dc.title","Connexin hemichannels in atrial fibrillation: orphaned and irrelevant?"],["dc.type","journal_article"],["dc.type.internalPublication","yes"],["dc.type.subtype","editorial_ja"],["dspace.entity.type","Publication"]]

[["dc.contributor.author","Peris-Yagüe, Víctor"],["dc.contributor.author","Rubio, Tony"],["dc.contributor.author","Fakuade, Funsho E."],["dc.contributor.author","Voigt, Niels"],["dc.contributor.author","Luther, Stefan"],["dc.contributor.author","Majumder, Rupamanjari"],["dc.date.accessioned","2022-02-23T16:37:04Z"],["dc.date.available","2022-02-23T16:37:04Z"],["dc.date.issued","2021"],["dc.identifier.doi","10.1101/2021.10.18.464761"],["dc.identifier.uri","https://resolver.sub.uni-goettingen.de/purl?gro-2/100399"],["dc.identifier.url","https://mbexc.uni-goettingen.de/literature/publications/416"],["dc.relation","EXC 2067: Multiscale Bioimaging"],["dc.relation.workinggroup","RG Voigt (Molecular Pharmacology)"],["dc.title","A mathematical model for electrical activity in pig atrial tissue"],["dc.type","preprint"],["dc.type.internalPublication","unknown"],["dspace.entity.type","Publication"]]