Inhaltspezifische Aktionen

Experimental Electrophysiology | AG Sossalla

Research Focus

The research group led by Prof. Sossalla focuses on investigating the impact of atrial fibrillation and pulmonary hypertension on right ventricular function. This work is part of subproject B10N within the Collaborative Research Center (CRC) 1213 “Pulmonary Hypertension and Cor Pulmonale,” funded by the Deutsche Forschungsgemeinschaft (DFG). In addition to electrophysiological techniques such as fluorescence microscopy and patch-clamp recordings, the group employs contractility assays using cultured myocardial slices as well as molecular biological approaches.

Human cardiac tissue, primarily obtained during heart transplantations, coronary artery bypass grafting, and valve surgeries, serves as the basis for these experiments. The aim of this translational project is to uncover the underlying mechanisms of right heart failure in the context of atrial fibrillation and pulmonary hypertension, and to contribute to the development of novel therapeutic strategies.

In addition, our group is engaged in research on the cardiorenal syndrome by examining the effects of kidney disease on human myocardial function.

Contact

Prof. Dr. med. Samuel T. Sossalla
Director of the Department of Internal Medicine I

DirektionMed1@uniklinikum-giessen.de

ORCID ID: 0000-0001-8034-2673

Team

Dr. med. Thomas Körtl
Clinical Scientist

Cardiorenal syndrome | Atrial fibrillation, pulmonary hypertension, and right ventricle

thomas.koertl@innere.med.uni-giessen.de

ORCID ID: 0009-0001-0776-3508

 

Dr. Mario Pavez-Giani
Junior Group Leader

Cardiac metabolism & Mitochondrial cardiomyopathy | Primary mitochondrial disease (nDNA and mtDNA mutations) in heart development, function and disease

mario.pavez-giani@uni-giessen.de

ORCID ID: 0000-0002-3330-9384

 

We are always seeking passionate and driven medical, master and PhD students who are interested in completing a thesis, and joining our translational research team. If a topic resonates with you, please do not hesitate to reach us out via email – we’d be happy to hear from you!

Publications

  1. Körtl T, Hankowitz N, Stengel L, et al. In Vitro Simulation of Hemodialysis Reveals Hemodialysis-Associated Pro-Arrhythmic Effects in a Human Cardiomyocyte Model. J Am Soc Nephrol. 2025;36(1):133-135. doi:10.1681/ASN.0000000563
  2. Pabel S, Knierim M, Stehle T, et al. Effects of Atrial Fibrillation on the Human Ventricle. Circ Res. 2022;130(7):994-1010. doi:10.1161/CIRCRESAHA.121.319718
  3. Bomer, N.*,Pavez-Giani*, M. G., Grote Beverborg, N., Cleland, J. G. F., van Veldhuisen, D. J., & van der Meer, P. (2022). Micronutrient deficiencies in heart failure: Mitochondrial dysfunction as a common pathophysiological mechanism?. Journal of internal medicine, 291(6), 713–731. https://doi.org/10.1111/joim.13456
  4. Körtl T, Stehle T, Riedl D, et al. Atrial Fibrillation Burden Specifically Determines Human Ventricular Cellular Remodeling. JACC Clin Electrophysiol. 2022;8(11):1357-1366. doi:10.1016/j.jacep.2022.07.016
  5. Pavez-Giani, M. G., & Cyganek, L. (2022). Recent Advances in Modeling Mitochondrial Cardiomyopathy Using Human Induced Pluripotent Stem Cells. Frontiers in cell and developmental biology, 9, 800529. https://doi.org/10.3389/fcell.2021.800529
  6. Bengel P, Dybkova N, Tirilomis P, et al. Detrimental proarrhythmogenic interaction of Ca2+/calmodulin-dependent protein kinase II and NaV1.8 in heart failure. Nat Commun. 2021;12(1):6586. doi:10.1038/s41467-021-26690-1
  7. Pavez-Giani, M. G., Sánchez-Aguilera, P. I., Bomer, N., Miyamoto, S., Booij, H. G., Giraldo, P., Oberdorf-Maass, S. U., Nijholt, K. T., Yurista, S. R., Milting, H., van der Meer, P., Boer, R. A., Heller Brown, J., Sillje, H. W. H., & Westenbrink, B. D. (2021). ATPase Inhibitory Factor-1 Disrupts Mitochondrial Ca2+ Handling and Promotes Pathological Cardiac Hypertrophy through CaMKIIδ. International journal of molecular sciences, 22(9), 4427. https://doi.org/10.3390/ijms22094427
  8. Bengel P, Ahmad S, Tirilomis P, et al. Contribution of the neuronal sodium channel NaV1.8 to sodium- and calcium-dependent cellular proarrhythmia. J Mol Cell Cardiol. 2020;144:35-46. doi:10.1016/j.yjmcc.2020.05.002
  9. Pabel S, Ahmad S, Tirilomis P, et al. Inhibition of NaV1.8 prevents atrial arrhythmogenesis in human and mice. Basic Res Cardiol. 2020;115(2):20. doi:10.1007/s00395-020-0780-8
  10. Pabel S, Wagner S, Bollenberg H, et al. Empagliflozin directly improves diastolic function in human heart failure. Eur J Heart Fail. 2018;20(12):1690-1700. doi:10.1002/ejhf.1328
  11. Hartmann N, Mason FE, Braun I, et al. The combined effects of ranolazine and dronedarone on human atrial and ventricular electrophysiology. J Mol Cell Cardiol. 2016;94:95-106. doi:10.1016/j.yjmcc.2016.03.012