Voigt, Niels, Prof. Dr.*

  • 2007: MD, Dresden University of Technology, Germany
  • 2008 – 2010: Postdoc at the Department of Pharmacology and Toxicology, Dresden University of Technology, Germany
  • 2010 – 2012: Postdoc at the Division of Experimental Cardiology, Medical Faculty Mannheim, Heidelberg University, Germany
  • 2012 – 2016: Postdoc at the Institute of Pharmacology, University of Duisburg-Essen, Germany
  • Since 2016: Professor and head of the Molecular Pharmacology Group at the Institute of Pharmacology and Toxicology, University Medical Center Göttingen, Germany

Major Research Interests

Atrial fibrillation (AF) is the most common cardiac arrhythmia and is associated with increased morbidity and mortality, particularly due to embolic stroke and heart failure. Current approaches to restore normal sinus rhythm (antiarrhythmic drugs, AF ablation) have major limitations including dissatisfying efficacy and risk of life-threatening proarrhythmic events. Therefore, we aim to unravel novel molecular mechanisms contributing to AF initiation and maintenance. In particular, we employ modern experimental techniques including cellular electrophysiology and calcium imaging to investigate atrial myocytes and tissue samples from patients undergoing open heart surgery. In addition, we utilize advanced techniques in the generation of atrial engineered heart tissue (aEHM) and modern gene editing approaches (CRISPR/Cas9) in order to develop new experimental models of AF. These approaches will provide the molecular basis for novel and patient-tailored therapeutic strategies for AF.

Homepage Department/Research Group


Selected Recent Publications

  • Voigt N, Maack C, Pronto JRD (2022). Targeting Mitochondrial Calcium Handling to Treat Atrial Fibrillation. J Am Coll Cardiol, 80(23):2220-3.

  • Seibertz F, Rapedius M, Fakuade FE, Tomsits P, Liutkute A, Cyganek L, Becker N, Majumder R, Clauß S, Fertig N, Voigt N (2022). A modern automated patch-clamp approach for high throughput electrophysiology recordings in native cardiomyocytes. Commun Biol, 5(1): 969.

  • Jung P, Seibertz F, Fakuade FE, Ignatyeva N, Sampathkumar S, Ritter M, Li H, Mason FE, Ebert A, Voigt N (2022). Increased cytosolic calcium buffering contributes to a cellular arrhythmogenic substrate in iPSC-cardiomyocytes from patients with dilated cardiomyopathy. Basic Res Cardiol, 117(1):5.

  • Fakuade EF, Steckmeister V, Seibertz F, Gronwald J, Kestel S, Menzel J, Pronto JRD, Taha K, Haghighi F, Kensah G, Pearman CM, Wiedmann F, Teske AJ, Schmidt C, Dibb KM, El-Essawi A, Danner BC, Baraki H, Schwappach B, Kutschka I, Mason FE, Voigt N (2020) Altered Atrial Cytosolic Calcium Handling Contributes to the Development of Postoperative Atrial Fibrillation. Cardiovasc Res, 117(7):1790-801.

  • Voigt N, Heijman J, Wang Q, Chiang DY, Li N, Karck M, Wehrens XHT, Nattel S, Dobrev D (2014) Cellular and molecular mechanisms of atrial arrhythmogenesis in patients with paroxysmal atrial fibrillation. Circulation, 129 (2): 145-56.

  • Voigt N, Li N, Wang Q, Wang W, Trafford AW, Abu-Taha I, Sun Q, Wieland T, Nattel S, Ravens U, Wehrens XHT, Dobrev D (2012) Enhanced sarcoplasmic reticulum Ca2+ leak and increased Na+-Ca2+ exchanger function underlie delayed afterdepolarizations in patients with chronic atrial fibrillation. Circulation, 125 (17): 2059-70.