Katrin Streckfuss-Bomeke

@university wuerzburg

Professor, Pharmacology and Toxicology/ University Medical centre Wuerzburg
Pharmacology and Toxicology

Katrin Streckfuss-Bomeke


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https://researchid.co/kboemek

RESEARCH, TEACHING, or OTHER INTERESTS

Cardiology and Cardiovascular Medicine, Pharmacology, Toxicology and Pharmaceutics, Cell Biology
84

Scopus Publications

Scopus Publications

  • Chamber-specific chromatin architecture guides functional interpretation of disease-associated Cis-regulatory elements in human cardiomyocytes
    S. Haydar, R. Bednarz, P. Laurette, I. Sobitov, N. Díaz i Pedrosa, P. Videm, T. Lueneburg, S. Kuß, H. Lahm, M. Dreßen, M. Krane, C. Schmidt, B. A. Grüning, N. Voigt, K. Streckfuss-Bömeke, R. Gilsbach
    Nature Communications, 2026
    Cis- regulatory elements (CREs) are noncoding DNA regions regulating cell-type-specific gene expression programs by interacting with distal gene promoters. Here, we aim to decode the function and spatial organization of CRE-promoter interactions in human cardiomyocytes. We analyzed the epigenome and chromatin interactions of human male atrial, ventricular, and failing cardiomyocytes. Atrial and ventricular cardiomyocytes harbored chamber-specific CRE-promoter interactions modulating gene expression as confirmed by functional epigenetic silencing. These CRE-promoter interactions explain the distinct contribution of non-coding genetic variants to atrial and ventricular diseases, such as dilated cardiomyopathy and arrhythmias. We dissected the prototypic KCNJ2 locus, encoding a potassium channel associated with ventricular arrhythmia susceptibility. Functional epigenetic silencing confirmed that CREs, harboring QT-duration-associated genetic risk factors, modulate KCNJ2 gene expression levels, alter KCNJ2-dependent channel currents, and affect cardiomyocyte repolarization. The presented human CM-specific chromatin interaction analysis provides key insights into regulatory mechanisms and aids in interpreting genetic risk factors.
  • Enhancing KLF15 activity in cardiomyocytes: a novel approach to prevent pathological reprogramming and fibrosis via nuclease-deficient dCas9VPR
    Eric Schoger, Rosa Kim, Federico Bleckwedel, Tomas Peralta, Laura Priesmeier, Janek Fischer, Laura Stengel, Cheila Rocha, Gabriela L. Santos, Susanne Lutz, Etienne Boileau, Nina Baumgarten, Marcel H. Schulz, Christoph Dieterich, Oliver J. Müller, Lukas Cyganek, Alfredo Cabrera-Orefice, Hanna Eberl, Christoph Maack, Katrin Streckfuss-Bömeke, Mario Pavez-Giani, Shirin Doroudgar, Samuel T. Sossalla, Laura C. Zelarayán
    Signal Transduction and Targeted Therapy, 2026
    Transcriptional activity perturbation holds promise for selectively modulating harmful transcriptional networks, but its therapeutic potential remains largely unexplored. We employed a network-based analysis of single-cell heart transcriptomes to identify transcription factor activities linked to pathological cardiomyocytes in vivo. This analysis revealed that transcriptional activity of Krüppel-like factor 15 (KLF15) exhibited the most significant change in pathological cardiomyocytes, characterized by less effective repression of disease-associated genes in stressed hearts, which correlated with reduced KLF15 expression. To restore KLF15 activity, we utilized CRISPR/nuclease-dead (d)Cas9-based transcriptional enhancement (CRISPRa) in cardiomyocytes, which effectively abolished fetal reprogramming by simultaneously suppressing pathological gene expression and restoring metabolic homeostasis under sustained stress conditions. Furthermore, we identified a novel cell-nonautonomous anti-fibrotic effect mediated by cardiomyocyte-fibroblast crosstalk, and revealed the contribution of KLF15-dependent Alpha-2-glycoprotein 1, zinc-binding (AZGP1) regulation in this process. We also elucidated the upstream mechanisms of KLF15 regulation, highlighting its role as a cell-specific downstream target of the broad TGF-β canonical signaling pathway, along with its downstream-dependent mechanisms in human cardiomyocytes. Finally, to enhance the therapeutic potential of this approach, we engineered and validated an adeno-associated viral (AAV) vector with a small CRISPRa system for endogenous regulation in human cardiomyocytes suitable for clinical applications. Overall, we elucidated a regulatory circuit involving TGF-β, KLF15, and AZGP1, which coordinates critical pathological responses through cellular crosstalk between cardiomyocytes and fibroblasts. Importantly, we demonstrated the efficacy of CRISPRa as an epigenetic intervention restoring a critical transcriptional function disrupted in non-genetic heart failure. This approach provides a promising blueprint for future adaptation targeting additional non-hereditary pathologies.
  • Generation of pluripotent stem cell line (IPWi001-A) and a corresponding CRISPR/Cas9 modified isogenic rescue control (IPWi001-A-1) from a patient with arrhythmia-induced cardiomyopathy harboring a KCNQ1 truncating mutation
    Meike Anders, Stefanie Hoppe, Hanna Eberl, Sabine Rebs, Aylin Seedorf, Wiebke Maurer, Tillmann Schill, Arne Zibat, Julia K. Unsöld, Gökhan Yigit, Bernd Wollnik, Dirk Vollmann, Samuel Sossalla, Katrin Streckfuss-Bömeke
    Stem Cell Research, 2026
    KCNQ1 functions as a slow rectifying potassium channel during the repolarization of the cardiac action potential, with mutations causing long-QT syndrome 1 and arrhythmias. A genetic link between KCNQ1 mutations and arrhythmia-induced cardiomyopathy (AIC) has not been identified, and the underlying pathways remain elusive. We generated human induced pluripotent stem cells (hiPSCs) from an AIC patient harboring the heterozygous truncating mutation p.W15* in KCNQ1 and corrected the mutation to wildtype using CRISPR/Cas9. The hiPSCs retained full pluripotency, genomic integrity, and differentiation ability. They were differentiated into hiPSC-cardiomyocytes (hiPSC-CM), establishing a patient-specific model to explore potential genetic connections to AIC.
  • Models of the human heart for biomedical research: Opportunities and challenges
    Katrin Streckfuss‐Bömeke, Laura C. Zelarayán, Renate B. Schnabel, Nicolle Kränkel, Christoph Maack, Thomas Eschenhagen, Hannah E. Kappler, Ursula Klingmüller, Rafael Kramann, Axel Loewe, Hendrik Milting, Cristina E. Molina, Daniela Panáková, Bruno K. Podesser, Angelika Schnieke, Katrin Schröder, Thomas Seidel, Samuel Sossalla, Callum Zgierski‐Johnston, Wolfram‐Hubertus Zimmermann, Eva A. Rog‐Zielinska, Peter Kohl
    Physiological Reports, 2026
    Model systems that mimic human cardiac structure and function are essential for the development of novel diagnostics and effective treatments for cardiovascular diseases. While non‐human vertebrate models, from zebrafish to pig, remain vital to cardiovascular research, the translatability of findings to human patients is often limited. Therefore, animal experiments should be supplemented with human model systems, including human induced pluripotent stem cell‐derived cells, 3D engineered constructs, and last but not least, native tissue preparations and isolated primary cardiomyocytes. However, while human myocardium remains the gold standard, human heart tissue – and particularly tissue from control hearts–remains scarce, and its use in research is generally restricted to settings where tissue has been excised from diseased or failing hearts. While it is in principle possible to use tissue from rejected non‐failing donor hearts that cannot be transplanted, legal hurdles (e.g., in Germany) can restrict the use of non‐transplanted donor organs in research. Given the challenges associated with accessing and using human tissue in biomedical research, an integrated strategy towards combining non‐human vertebrate models, in silico models, and human tissue‐derived models is recommended, enhancing the chances of successful research and development, and helping bridge the gap between preclinical and clinical research.
  • Cardiac arrhythmias—Cellular mechanisms, consequences and challenges in the diagnostics using human models
    Katrin Streckfuß-Bömeke, Christoph Maack, Samuel Sossalla
    Herz, 2026
  • A human-on-human assay for detecting anti-myocardial antibodies in patients with myocardial disease
    Anne Auer, Johanna Siegel, Stasa Janjatovic, Margarete Heinrichs, Stefan Störk, Peter Heuschmann, Caroline Morbach, Katrin Streckfuss-Bömeke, Gustavo C. Ramos, Katrin G. Heinze
    Frontiers in Immunology, 2026
    Adaptive immune responses, particularly the production of anti-myocardial antibodies, have been implicated as critical mediators in myocardial healing and remodeling following myocardial infarction (MI), acute myocarditis (Myo), and heart failure (HF). However, current methods for detecting heart-reactive antibodies in patients are insufficient, as most rely on heart tissue slices from primates or other species. These approaches pose technical, logistical, and ethical challenges, including the risk of false negative results due to lack of inter-species cross-reactivity. To address these limitations, we developed a human cell-based assay to screen for patient-derived serum or plasma reactivity against human cardiomyocytes differentiated from induced pluripotent stem cells (iPSC-CMs). This human-on-human test system can detect cardiomyocyte-specific immunoglobulins present in patient plasma by applying indirect immunofluorescence staining, followed by convenient visualization through either confocal microscopy or standard widefield systems available in clinical laboratories. Overall, this approach provides a physiologically relevant and ethically responsible model for rapid, accurate testing of anti-myocardial antibodies across various clinical settings, thus offering accessible tools to stratify patients with myocardial disease according to their adaptive immune response status.
  • Deregulation of m6A-RNA methylation impairs adaptive hypertrophic response and drives maladaptation via mTORC1-S6K1-hyperactivation and autophagy impairment
    Karthika Annamalai, Soniya Dilliker, Eric Buchholz, Ricardo Castro-Hernández, Nikita Panyam, Alessa Pommeranz, Pascal Wiederhake, Nelly Wery von Limont, Nina Hempel, Verena Ebner, Surabhi Swarnkar, Belal A. Mohamed, Katrin Streckfuss-Bömeke, Sabine Steffens, Stephan Herzig, Antje Ebert, Andre Fischer, Karl Toischer
    Cell Communication and Signaling, 2025
    Pressure overload first leads to compensated hypertrophy and secondary to heart failure. m6A-RNA methylation is a fast process for the adaptation of cell composition. m6A-RNA-methylation is regulated by the demethylase, fat mass and obesity-associated protein ( FTO), and FTO protein levels are diminished in heart failure. Cardiomyocyte-specific FTO-transgenic/knockout-mice have shown the relevance of FTO in pressure overload remodeling. However, its functional downstream regulatory mechanisms are still unclear. In this study, we discover the harmful signaling pathways that are triggered by m6A imbalance and FTO loss, which eventually lead to adverse cardiac remodeling and heart failure. FTOcKO animals were generated by crossing FTO fl/fl mice with \(\alpha\) - MHC Cre mice using Cre-lox system. Control and the FTOcKO animals groups were subjected to TAC (transverse aortic constriction) surgery. Echocardiography was performed 1-week post-TAC surgery. MeRIP (m6A RNA immunoprecipitation) sequencing was performed from the heart tissues of mice after one week TAC surgery. Additionally, the mechanistical interrelation between the signaling pathways during FTO loss and adverse cardiac remodeling were investigated in human iPS-CMs (hiPS-CMs). One week post-TAC surgery, FTOcKO mice showed impaired cardiac function (EF: CreC TAC (45%) vs. FTOcKO TAC (25%), p < 0.0001) and increased LVID (CreC TAC(3.9 mm) vs. FTOcKO TAC (4.8 mm), p < 0.0001), indicating a lack of adaption to pressure overload. Knockdown of FTO in hiPS-cardiomyocytes also reduced endothelin-induced hypertrophic response. MeRIP-seq data of FTOcKO mice showed that the differentially hypermethylated transcripts were associated with cardiac apoptosis inhibition (CDK1, CFLAR), mTORC1 signaling pathway (AKT1S1) and autophagy regulation (TFEB). mTORC1 was identified as a central player of dysregulation with hyperactivation of its canonical substrates phospho-S6K1 (Thr 389) and phospho-S6 (ser235/236) ex-vivo (FTOcKO) and in-vitro (FTO-KD-hiPS-CMs). Moreover, FTO-deficient cardiomyocytes cause autophagic flux impairment and defective autophagy. The effect of atrophy and induced apoptosis upon FTO-m6A imbalance could be rescued by pharmacological inhibiton of the mTORC1-S6K1 pathway. Downregulation of FTO leads to mTORC1-S6K1 hyperactivation that shift the compensative hypertrophic response to atrophy and apoptosis leading to progressive heart failure. These findings might pave the way for the development of novel therapeutic targets for the early phases of heart failure treatments.
  • Impaired Atrial Mitochondrial Calcium Handling in Patients With Atrial Fibrillation
    Julius Ryan D. Pronto, Fleur E. Mason, Eva A. Rog-Zielinska, Funsho E. Fakuade, Donata Bülow, Marcell Tóth, Khaled Machwart, Paulina Brandes, Felix Wiedmann, Michael Kohlhaas, Alexander Nickel, Matthias Wolf, Julian Mustroph, Kim-Chi Vu, Sören Brandenburg, Tri Q. Do, Peter Joshua Siedler, Katharina Ritzenhoff, Zongqian Xue, Xiaobo Zhou, Stefanie Kestel, Olga Dschun, Oksana Kyshynska, George Kensah, Robyn T. Rebbeck, Aschraf El-Essawi, Ahmad Fawad Jebran, Bernhard C. Danner, Hassina Baraki, Johann Schredelseker, Ivan Bogeski, Bianca J.J.M. Brundel, Stephan E. Lehnart, Constanze Bening, Ingo Kutschka, Felix Bremmer, Stefan M. Kallenberger, Silvio O. Rizzoli, Björn C. Knollmann, Stefan Neef, Katrin Streckfuss-Bömeke, Constanze Schmidt, Christoph Maack, Niels Voigt
    Circulation Research, 2025
    BACKGROUND: Mitochondrial calcium (Ca 2+ ) is a key regulator of cardiac energetics by stimulating the tricarboxylic acid cycle during elevated workload. Atrial fibrillation (AF) is associated with a reduction in cytosolic Ca 2+ transient amplitude, but its effect on mitochondrial Ca 2+ handling and cellular redox state has not been explored. METHODS: Cardiac myocytes isolated from patient-derived right atrial biopsies were subjected to workload transitions using patch-clamp stimulation and β-adrenergic stimulation (isoproterenol). In conjunction, nicotinamide adenine dinucleotide (phosphate)/flavin adenine dinucleotide (NAD[P]H/FAD) autofluorescence, cytosolic and mitochondrial [Ca 2+ ] were monitored using epifluorescence microscopy. Sarcoplasmic reticulum and mitochondria were imaged using electron microscopy and tomography and stimulated emission depletion microscopy. The effects of the mitochondrial Ca 2+ uptake enhancer ezetimibe on proarrhythmic activity in atrial myocytes and on AF burden in patients were investigated. RESULTS: Mitochondrial Ca 2+ accumulation during increased workload was blunted in AF, and was associated with impaired regeneration of nicotinamide adenine dinucleotide and flavin adenine dinucleotide. Nanoscale imaging revealed spatial disorganization of sarcoplasmic reticulum and mitochondria, associated with microtubule destabilization. This was confirmed in human induced pluripotent stem cell–derived cardiac myocytes, where treatment with the microtubule destabilizer nocodazole displaced mitochondria and increased proarrhythmic Ca 2+ sparks, which were rescued by MitoTEMPO. Ezetimibe also reduced the occurrence of arrhythmogenic Ca 2+ release events both in AF myocytes and nocodazole-treated human induced pluripotent stem cell–derived cardiac myocytes. Retrospective patient analysis also revealed a reduced AF burden in patients on ezetimibe treatment. CONCLUSIONS: Mitochondrial Ca 2+ uptake and accumulation are impaired in atrial myocytes from patients with AF. The disturbed spatial association between sarcoplasmic reticulum and mitochondria driven by destabilized microtubules may underlie impaired Ca 2+ transfer in AF. Enhancing mitochondrial Ca 2+ uptake potentially protects against arrhythmogenic events.
  • Arrhythpy: an automated tool to quantify and classify arrhythmias in Ca2+ transients of iPSC-cardiomyocytes
    Karim Ajmail, Charlotte Brand, Thomas Borchert, Benjamin Meder, Sabine Rebs, Katrin Streckfuss-Bömeke
    American Journal of Physiology Heart and Circulatory Physiology, 2025
    Arrhythmias in calcium transients are easy to detect by human perception. However, quantifying these arrhythmias in a computer-readable manner remains challenging. To address this, we developed Arrhythpy, an automated tool that measures arrhythmias in iPSC-derived cardiomyocytes by analyzing Ca2+ transients. Unlike other tools, Arrhythpy directly evaluates arrhythmia levels. It effectively monitors arrhythmias in healthy and diseased iPSC-CMs, including dilated cardiomyopathy and Takotsubo syndrome. Arrhythpy’s flexible framework suits varied cell types and measurement techniques.
  • Atrial fibrillation in end-stage heart failure: Cellular mechanisms behind CASTLE-HTx
    Maria Knierim, Nico Hartmann, Wiebke Maurer, Steffen Pabel, Simon Sedej, Dirk von Lewinski, Jan Gummert, Christian Sohns, Katrin Streckfuss‐Bömeke, Samuel Sossalla
    European Journal of Heart Failure, 2025
    Atrial fibrillation (AF) often coexists in patients with heart failure (HF). Rhythm restoration is increasingly recognized as a prognostically relevant strategy in patients with HF and AF. However, compared to other frequent comorbidities like chronic kidney disease or type 2 diabetes, the reciprocal interaction between HF and AF and particularly the impact of AF on the development and progression of HF has not been fully understood and continues to be underestimated.1 Recently, the CASTLE-HTx trial, among others, demonstrated that catheter ablation for AF and the reduction of AF burden improved prognosis even in patients with end-stage HF. This was associated with improved left ventricular systolic function following AF ablation.1-3 Those results clearly underscore the need to explore the largely unknown mechanisms of AF in end-stage HF. To investigate the effects of persisting AF on ventricular function in severe HF, we isolated 15 human ventricular trabeculae from freshly explanted end-stage HF hearts from nine patients in total and seven trabeculae from four non-HF organ donors (non-failing [NF]) as described previously.4 NF samples were acquired from patients whose hearts could not be transplanted due to non-cardiac medical or technical reasons. The cohort of HF patients had a mean age of 60.4 ± 1.6 years (mean ± standard error of the mean), left ventricular ejection fraction of 28.0 ± 3.2% and ischaemic cardiomyopathy in 44.4% of cases. All patients received guideline-directed medical therapy with no significant differences. The isolated trabeculae were subjected to AF simulation by electric stimulation in vitro for up to 8 h using a purpose-made pacing system (C-Pace EM, IonOptix, Westwood, MA, USA) with irregular stimulation intervals (60 bpm with 40% beat-to-beat variability) versus control stimulation (60 bpm with regular intervals). Contractility was assessed at 60 bpm in each group at baseline and intermittently after 2, 4, and 8 h of continuous pacing. To investigate cellular mechanisms of AF in human HF, we utilized a total of nine differentiations of human induced pluripotent stem cell-derived cardiomyocytes (hiPSC-CM) generated from two patients with familial dilated cardiomyopathy (DCM) with end-stage HF and three differentiations from one healthy control patient.5 Cardiomyocyte (CM) differentiation and cell culture were performed as previously described.5, 6 Chronic AF simulation for 48 h was performed by continuous pacing of hiPSC-CM in culture using the C-Pace EM pacing system (90 bpm with 30% beat-to-beat variability vs. regular 60 bpm). Intracellular Ca2+ cycling was studied in DCM and healthy hiPSC-CM after 48 h of AF simulation using the Ca2+ sensitive dye Fura-2 as described elsewhere.6 The patch-clamp method in voltage-clamp mode was employed to record action potentials (AP) in DCM and healthy hiPSC-CM after 48 h of AF or control stimulation, following an established protocol.6 All procedures were performed according to the Declaration of Helsinki and were approved by the local ethics committees of the University of Göttingen (ref. no. 10/9/15, 31/9/00) and Medical University of Graz (ref. no. 28-508 ex 15/16). Atrial fibrillation simulation for 8 h resulted in a substantial decrease in systolic contractile force in human end-stage HF trabeculae compared to control (Figure 1). Furthermore, diastolic function rapidly deteriorated due to AF simulation, as represented by a significant increase in diastolic tension and slowed relaxation compared to control stimulation (Figure 1). In contrast, trabeculae from NF hearts did not exhibit a negative contractile response to AF simulation (Figure 1), demonstrating the rapid deterioration of ventricular function solely because of AF in pre-existing HF. Ca2+ cycling measurements were performed in DCM and healthy hiPSC-CM after 48 h of AF simulation or rhythmic control stimulation to investigate potential underlying cellular mechanisms. Continuous AF simulation for 48 h in DCM hiPSC-CM resulted in a substantial reduction of systolic Ca2+ release compared to control stimulation, as measured by reduced Ca2+ transient amplitude (Figure 1). Concomitantly, the intracellular Ca2+ elimination in diastole (elimination constant τ) was significantly slower after AF simulation than upon control stimulation in DCM hiPSC-CM (Figure 1). The latter was likely related to a reduction in SERCA2a activity after AF simulation, leading to slower Ca2+ reuptake to the sarcoplasmic reticulum as evaluated by rapid high-dose caffeine application (Figure 1). Again, these effects could not be observed in healthy hiPSC-CM after 48 h of AF simulation (Figure 1). Furthermore, patch-clamp experiments in DCM hiPSC-CM revealed a significant prolongation of the AP duration (90%) after 48 h of AF simulation compared to rhythmic stimulation in DCM hiPSC-CM, but not in healthy hiPSC-CM (Figure 1). These effects altogether illustrate the detrimental impact of AF on human failing myocardium compared to healthy myocardium. Our translational human myocardium-based experiments demonstrate that AF leads to rapid and severe ventricular contractile dysfunction and cellular functional remodelling in human HF. As Ca2+ is a major determinant of myocardial contractile function, this could be explained mechanistically by adverse Ca2+ cycling alterations in DCM hiPSC-CM in early stages of AF simulation. Furthermore, AF simulation induced a distinct prolongation of the AP in hiPSC-CM, which constitutes an electrophysiological hallmark of HF. Interestingly, in NF myocardium and healthy hiPSC-CM, these effects could not be observed. Recent experimental work from our group has shown similar HF-typical effects of long-term AF simulation on Ca2+ handling and AP morphology, although only after a longer period of AF simulation of 7 days in healthy CM.6, 7 Mechanistically, increased production of reactive oxygen species with oxidative regulation of Ca2+/calmodulin-dependent protein kinase II (CaMKII), along with differential regulation of proteins involved in Ca2+ homeostasis (e.g. reduction of SERCA2a activity) and electrophysiology, have been demonstrated as causal mechanisms for the observed alterations.6 Supporting this pathway and the importance of AF-induced alterations, increased CaMKII and AMP-activated protein kinase activity after AF simulation have been associated with Ca2+ cycling alterations and disturbed fatty acid and glucose metabolism, accompanied by pro-apoptotic pathways in a neonatal rat-CM model.8 Most noteworthy, we here demonstrate that in pre-existing HF adverse effects of AF on myocardial function can be observed earlier and to a greater extent than in healthy myocardium. This highlights the vulnerability of HF ventricular myocardium towards AF and, in context with recent clinical studies like CASTLE-AF or CASTLE-HTx, underscores the importance of timely rhythm restoration and AF burden reduction in pre-existing HF. We gratefully acknowledge the expert technical assistance of Y. Metz, J. Heine and D. Riedl. Open Access funding enabled and organized by Projekt DEAL. S.P. is funded by the Else-Kröner-Fresenius Stiftung and by the German Heart Foundation/German Foundation of Heart Research. K.S.B. and S.S. are funded by the Deutsche Forschungsgemeinschaft (DFG) through the research grant SO 1223/4-1 and the F. Thyssen Foundation (Az 10.19.2.026MN), and projects B10N&B07 of the Collaborative Research Center 1213-Pulmonary Hypertension and Cor Pulmonale DFG. Conflict of interest: K.S.B. reports research support from Novartis and BionTECH and speaker's honoraria from Novartis, outside of the submitted manuscript. S.S. reports speaker's/consultancy honoraria from Boehringer Ingelheim, AstraZeneca, Berlin-Chemie, Novartis, Bristol Myers Squibb, and Lilly. All other authors have nothing to disclose.
  • Mechano-energetic uncoupling in heart failure
    Dunja Aksentijevic, Simon Sedej, Jeremy Fauconnier, Melanie Paillard, Mahmoud Abdellatif, Katrin Streckfuss-Bömeke, Renée Ventura-Clapier, Jolanda van der Velden, Rudolf A. de Boer, Edoardo Bertero, Jan Dudek, Vasco Sequeira, Christoph Maack
    Nature Reviews Cardiology, 2025
  • Mitochondrial targets in ischaemic heart disease and heart failure, and their potential for a more efficient clinical translation. A scientific statement of the ESC Working Group on Cellular Biology of the Heart and the ESC Working Group on Myocardial Function
    Melanie Paillard, Mahmoud Abdellatif, Ioanna Andreadou, Christian Bär, Luc Bertrand, Bianca J.J.M. Brundel, Gemma Chiva‐Blanch, Sean M. Davidson, Dana Dawson, Fabio Di Lisa, Paul Evans, Zoltan Giricz, Derek J. Hausenloy, Petra Kleinbongard, Frank Lezoualc'h, Elisa Liehn, Christoph Maack, Ange Maguy, Elizabeth Murphy, Cinzia Perrino, Maurizio Pesce, Peter P. Rainer, Katrin Streckfuss‐Bömeke, Matthias Thielmann, Rong Tian, Carlo G. Tocchetti, Jolanda Van Der Velden, Sophie Van Linthout, Serena Zacchigna, Thomas Krieg
    European Journal of Heart Failure, 2025
  • Update on preclinical models of cancer therapy-related cardiac dysfunction: Challenges and perspectives. A scientific statement of the Heart Failure Association (HFA) of the ESC, the ESC Council of Cardio-Oncology, and the ESC Working Group on Cellular Biology of the Heart
    Alessandra Ghigo, Pietro Ameri, Aarti Asnani, Edoardo Bertero, Rudolf A. de Boer, Dimitrios Farmakis, Arantxa González, Stephane Heymans, Borja Ibáñez, Teresa López‐Fernández, Alexander R. Lyon, Piero Pollesello, Amina Rakisheva, Konstantinos Stellos, Katrin Streckfuss‐Bömeke, Carlo Gabriele Tocchetti, Thomas Thum, Peter van der Meer, Eva Van Rooij, Piotr Ponikowski, Marco Metra, Giuseppe Rosano, Sophie Van Linthout
    European Journal of Heart Failure, 2025
  • Opportunities and challenges for the use of human samples in translational cardiovascular research: a scientific statement of the ESC Working Group on Cellular Biology of the Heart, the ESC Working Group on Cardiovascular Surgery, the ESC Council on Basic Cardiovascular Science, the ESC Scientists of Tomorrow, the European Association of Percutaneous Cardiovascular Interventions of the ESC, and the Heart Failure Association of the ESC
    Sean M Davidson, Ioanna Andreadou, Charalambos Antoniades, Jozef Bartunek, Cristina Basso, Bianca J J M Brundel, Robert A Byrne, Gemma Chiva-Blanch, Paula da Costa Martins, Paul C Evans, Henrique Girão, Zoltan Giricz, Can Gollmann-Tepeköylü, Tomasz Guzik, Mariann Gyöngyösi, Norbert Hübner, Michael Joner, Petra Kleinbongard, Thomas Krieg, Elisa Liehn, Rosalinda Madonna, Ange Maguy, Melanie Paillard, Maurizio Pesce, Steffen E Petersen, Gabriele G Schiattarella, Joost P G Sluijter, Sabine Steffens, Katrin Streckfuss-Bömeke, Matthias Thielmann, Art Tucker, Sophie Van Linthout, William Wijns, Johann Wojta, Joseph C Wu, Cinzia Perrino
    Cardiovascular Research, 2025
  • In Vitro Simulation of Hemodialysis Reveals Hemodialysis-Associated Pro-Arrhythmic Effects in a Human Cardiomyocyte Model
    Thomas Körtl, Niklas Hankowitz, Laura Stengel, Oliver Pfeuffer, Dominic Riedl, Frank Schweda, Katrin Streckfuß-Bömeke, Samuel Sossalla
    Journal of the American Society of Nephrology, 2025
  • State of the art and perspectives of gene therapy in heart failure. A scientific statement of the Heart Failure Association of the ESC, the ESC Council on Cardiovascular Genomics and the ESC Working Group on Myocardial & Pericardial Diseases
    Sophie Van Linthout, Konstantinos Stellos, Mauro Giacca, Edoardo Bertero, Antonio Cannata, Lucie Carrier, Pablo Garcia‐Pavia, Alessandra Ghigo, Arantxa González, Kristina H. Haugaa, Massimo Imazio, Luis R. Lopes, Patrick Most, Piero Pollesello, Heribert Schunkert, Katrin Streckfuss‐Bömeke, Thomas Thum, Carlo Gabriele Tocchetti, Carsten Tschöpe, Peter van der Meer, Eva van Rooij, Marco Metra, Giuseppe M.C. Rosano, Stephane Heymans
    European Journal of Heart Failure, 2025
  • Methamphetamine-induced cardiotoxicity: in search of protective transcriptional mechanisms
    Kristin Annawald, Katrin Streckfuss-Bömeke, Thomas Meyer
    Herz, 2024
  • Generation of a heterozygous Calsequestrin 2 F189L iPSC line (UMGi158-B) by CRISPR/Cas9 genome editing to investigate the cardiac pathophysiology of Takotsubo Syndrome and Catecholaminergic Polymorphic Ventricular Tachycardia
    Gideon Syed Ali, Sabine Rebs, Hanna Eberl, Clarissa Zinke, Daniela Hübscher, Wiebke Maurer, Alexandra Busley, Lukas Cyganek, Katrin Streckfuss-Bömeke
    Stem Cell Research, 2024
  • Epigenetic modulators link mitochondrial redox homeostasis to cardiac function in a sex-dependent manner
    Zaher ElBeck, Mohammad Bakhtiar Hossain, Humam Siga, Nikolay Oskolkov, Fredrik Karlsson, Julia Lindgren, Anna Walentinsson, Dominique Koppenhöfer, Rebecca Jarvis, Roland Bürli, Tanguy Jamier, Elske Franssen, Mike Firth, Andrea Degasperi, Claus Bendtsen, Robert I. Menzies, Katrin Streckfuss-Bömeke, Michael Kohlhaas, Alexander G. Nickel, Lars H. Lund, Christoph Maack, Ákos Végvári, Christer Betsholtz
    Nature Communications, 2024
  • Cellular calcium handling and electrophysiology are modulated by chronic physiological pacing in human induced pluripotent stem cell-derived cardiomyocytes
    Maria Knierim, Thea Bommer, Michael Paulus, Dominic Riedl, Sarah Fink, Arnold Pöppl, Florian Reetz, Peter Wang, Lars S. Maier, Niels Voigt, Matthias Nahrendorf, Samuel Sossalla, Katrin Streckfuss-Bömeke, Steffen Pabel
    American Journal of Physiology Heart and Circulatory Physiology, 2024
  • Physiologists as medical scientists: An early warning from the German academic system
    Katrin Streckfuss‐Bömeke, Nicolle Kränkel, Christoph Maack, Renate B. Schnabel, Laura C. Zelarayán, Norbert Frey, Peter Jezzard, Martina Krüger, Nico Lachmann, Susanne Lutz, Claudia Noack, Eric Schoger, Katrin Schröder, Laura C. Sommerfeld, Sabine Steffens, Holger Winkels, Christina Würtz, Tanja Zeller, Eva A. Rog‐Zielinska, Peter Kohl
    Physiological Reports, 2024
  • Simulation of cardiac arrhythmias in human induced pluripotent stem cell-derived cardiomyocytes
    Thea Bommer, Maria Knierim, Julia Unsöld, Dominic Riedl, Laura Stengel, Michael Paulus, Thomas Körtl, Norman Liaw, Lars S. Maier, Katrin Streckfuss-Bömeke, Samuel Sossalla, Steffen Pabel
    Plos One, 2024
  • Generation of a pluripotent stem cell line (UMGi270-A) and a corresponding CRISPR/Cas9 modified isogenic control (UMGi270-A-1) from a patient with sudden onset dilated cardiomyopathy harboring a FLNC p.R2187P mutation
    Wiebke Maurer, Sabine Rebs, Steffen Köhne, Hanna Eberl, Bernd Wollnik, Arne Zibat, Katrin Streckfuss-Bömeke
    Stem Cell Research, 2024
  • NaV1.8 as Proarrhythmic Target in a Ventricular Cardiac Stem Cell Model
    N. Hartmann, M. Knierim, W. Maurer, N. Dybkova, Florian Zeman, Gerd Hasenfuss, S. Sossalla, K. Streckfuss-Bömeke
    International Journal of Molecular Sciences, 2024
  • The challenges of research data management in cardiovascular science: a DGK and DZHK position paper—executive summary
    Sabine Steffens, Katrin Schröder, Martina Krüger, Christoph Maack, Katrin Streckfuss-Bömeke, Johannes Backs, Rolf Backofen, Bettina Baeßler, Yvan Devaux, Ralf Gilsbach, Jordi Heijman, Jochen Knaus, Rafael Kramann, Dominik Linz, Allyson L. Lister, Henrike Maatz, Lars Maegdefessel, Manuel Mayr, Benjamin Meder, Sara Y. Nussbeck, Eva A. Rog-Zielinska, Marcel H. Schulz, Albert Sickmann, Gökhan Yigit, Peter Kohl
    Clinical Research in Cardiology, 2024
  • Generation of an RBM20-mutation-associated left-ventricular non-compaction cardiomyopathy iPSC line (UMGi255-A) into a DCM genetic background to investigate monogenetic cardiomyopathies
    Hanna Eberl, Sabine Rebs, Stefanie Hoppe, Farbod Sedaghat-Hamedani, Elham Kayvanpour, Benjamin Meder, Katrin Streckfuss-Bömeke
    Stem Cell Research, 2024
  • Electrophysiological and calcium-handling development during long-term culture of human-induced pluripotent stem cell-derived cardiomyocytes
    Fitzwilliam Seibertz, Henry Sutanto, Rebekka Dülk, Julius Ryan D. Pronto, Robin Springer, Markus Rapedius, Aiste Liutkute, Melanie Ritter, Philipp Jung, Lea Stelzer, Luisa M. Hüsgen, Marie Klopp, Tony Rubio, Funsho E. Fakuade, Fleur E. Mason, Nico Hartmann, Steffen Pabel, Katrin Streckfuss-Bömeke, Lukas Cyganek, Samuel Sossalla, Jordi Heijman, Niels Voigt
    Basic Research in Cardiology, 2023
  • Activation of the integrated stress response rewires cardiac metabolism in Barth syndrome
    Ilona Kutschka, Edoardo Bertero, Christina Wasmus, Ke Xiao, Lifeng Yang, Xinyu Chen, Yasuhiro Oshima, Marcus Fischer, Manuela Erk, Berkan Arslan, Lin Alhasan, Daria Grosser, Katharina J. Ermer, Alexander Nickel, Michael Kohlhaas, Hanna Eberl, Sabine Rebs, Katrin Streckfuss-Bömeke, Werner Schmitz, Peter Rehling, Thomas Thum, Takahiro Higuchi, Joshua Rabinowitz, Christoph Maack, Jan Dudek
    Basic Research in Cardiology, 2023
  • Atrial fibrillation-Associated electrical remodelling in human induced pluripotent stem cell-derived atrial cardiomyocytes: A novel pathway for antiarrhythmic therapy development
    Fitzwilliam Seibertz, Tony Rubio, Robin Springer, Fiona Popp, Melanie Ritter, Aiste Liutkute, Lena Bartelt, Lea Stelzer, Fereshteh Haghighi, Jan Pietras, Hendrik Windel, Núria Díaz i Pedrosa, Markus Rapedius, Yannic Doering, Richard Solano, Robin Hindmarsh, Runzhu Shi, Malte Tiburcy, Tobias Bruegmann, Ingo Kutschka, Katrin Streckfuss-Bömeke, George Kensah, Lukas Cyganek, Wolfram H Zimmermann, Niels Voigt
    Cardiovascular Research, 2023
  • An interferon gamma response signature links myocardial aging and immunosenescence
    DiyaaElDin Ashour, Sabine Rebs, Panagiota Arampatzi, Antoine-Emmanuel Saliba, Jan Dudek, Richard Schulz, Ulrich Hofmann, Stefan Frantz, Clément Cochain, Katrin Streckfuß-Bömeke, Gustavo Campos Ramos
    Cardiovascular Research, 2023
  • Molecular and Functional Relevance of NaV1.8-Induced Atrial Arrhythmogenic Triggers in a Human SCN10A Knock-Out Stem Cell Model
    Nico Hartmann, Maria Knierim, Wiebke Maurer, Nataliya Dybkova, Gerd Hasenfuß, Samuel Sossalla, Katrin Streckfuss-Bömeke
    International Journal of Molecular Sciences, 2023
  • Large-scale microRNA functional high-throughput screening identifies miR-515-3p and miR-519e-3p as inducers of human cardiomyocyte proliferation
    Harsha V. Renikunta, Katina Lazarow, Yiqi Gong, Praphulla Chandra Shukla, Vanasa Nageswaran, Hector Giral, Adelheid Kratzer, Lennart Opitz, Felix B. Engel, Arash Haghikia, Sarah Costantino, Francesco Paneni, Jens Peter von Kries, Katrin Streckfuss-Bömeke, Ulf Landmesser, Philipp Jakob
    Iscience, 2023
  • Moving toward gender equity in the cardiology and cardiovascular research workforce in Germany: a report from the German Cardiac Society
    Carolin Lerchenmüller, Laura Zelarayan, Katrin Streckfuss-Bömeke, Maria Rubini Gimenez, Renate Schnabel, Djawid Hashemi, Stephan Baldus, Tanja K Rudolph, Caroline Morbach
    European Heart Journal Open, 2023
  • A novel single-cell RNA-sequencing approach and its applicability connecting genotype to phenotype in ageing disease
    Orr Shomroni, Maren Sitte, Julia Schmidt, Sabnam Parbin, Fabian Ludewig, Gökhan Yigit, Laura Cecilia Zelarayan, Katrin Streckfuss-Bömeke, Bernd Wollnik, Gabriela Salinas
    Scientific Reports, 2022
  • Tachycardiomyopathy entails a dysfunctional pattern of interrelated mitochondrial functions
    Michael G. Paulus, Kathrin Renner, Alexander G. Nickel, Christoph Brochhausen, Katharina Limm, Elmar Zügner, Maria J. Baier, Steffen Pabel, Stefan Wallner, Christoph Birner, Andreas Luchner, Christoph Magnes, Peter J. Oefner, Klaus J. Stark, Stefan Wagner, Christoph Maack, Lars S. Maier, Katrin Streckfuss-Bömeke, Samuel Sossalla, Alexander Dietl
    Basic Research in Cardiology, 2022
  • Reduction of A-to-I RNA editing in the failing human heart regulates formation of circular RNAs
    Karoline E. Kokot, Jasmin M. Kneuer, David John, Sabine Rebs, Maximilian N. Möbius-Winkler, Stephan Erbe, Marion Müller, Michael Andritschke, Susanne Gaul, Bilal N. Sheikh, Jan Haas, Holger Thiele, Oliver J. Müller, Susanne Hille, Florian Leuschner, Stefanie Dimmeler, Katrin Streckfuss-Bömeke, Benjamin Meder, Ulrich Laufs, Jes-Niels Boeckel
    Basic Research in Cardiology, 2022
  • Doxorubicin induces cardiotoxicity in a pluripotent stem cell model of aggressive B cell lymphoma cancer patients
    Luis Peter Haupt, Sabine Rebs, Wiebke Maurer, Daniela Hübscher, Malte Tiburcy, Steffen Pabel, Andreas Maus, Steffen Köhne, Rewati Tappu, Jan Haas, Yun Li, Andre Sasse, Celio C. X. Santos, Ralf Dressel, Leszek Wojnowski, Gertrude Bunt, Wiebke Möbius, Ajay M. Shah, Benjamin Meder, Bernd Wollnik, Samuel Sossalla, Gerd Hasenfuss, Katrin Streckfuss-Bömeke
    Basic Research in Cardiology, 2022
  • Atrial Fibrillation Burden Specifically Determines Human Ventricular Cellular Remodeling
    Thomas Körtl, Thea Stehle, Dominic Riedl, Johanna Trausel, Sabine Rebs, Steffen Pabel, Michael Paulus, Andreas Holzamer, Nassir Marrouche, Lars S. Maier, Christian Sohns, Katrin Streckfuss-Bömeke, Samuel Sossalla
    Jacc Clinical Electrophysiology, 2022
  • Genotype Complements the Phenotype: Identification of the Pathogenicity of an LMNA Splice Variant by Nanopore Long-Read Sequencing in a Large DCM Family
    Farbod Sedaghat-Hamedani, Sabine Rebs, Elham Kayvanpour, Chenchen Zhu, Ali Amr, Marion Müller, Jan Haas, Jingyan Wu, Lars M. Steinmetz, Philipp Ehlermann, Katrin Streckfuss-Bömeke, Norbert Frey, Benjamin Meder
    International Journal of Molecular Sciences, 2022
  • Generation of homozygous Nav1.8 knock-out iPSC lines by CRISPR Cas9 genome editing to investigate a potential new antiarrhythmic strategy
    Wiebke Maurer, Nico Hartmann, Loukas Argyriou, Samuel Sossalla, Katrin Streckfuss-Bömeke
    Stem Cell Research, 2022
  • Effects of Atrial Fibrillation on the Human Ventricle
    Steffen Pabel, Maria Knierim, Thea Stehle, Felix Alebrand, Michael Paulus, Marcel Sieme, Melissa Herwig, Friedrich Barsch, Thomas Körtl, Arnold Pöppl, Brisca Wenner, Senka Ljubojevic-Holzer, Cristina E. Molina, Nataliya Dybkova, Daniele Camboni, Thomas H. Fischer, Simon Sedej, Daniel Scherr, Christof Schmid, Christoph Brochhausen, Gerd Hasenfuß, Lars S. Maier, Nazha Hamdani, Katrin Streckfuss-Bömeke, Samuel Sossalla
    Circulation Research, 2022
  • A quantitative RT-PCR protocol to adapt and quantify RBM20-dependent exon splicing of targets at the human locus
    Sabine Rebs, Tjark Alexander Buchwald, Katrin Streckfuss-Bömeke
    STAR Protocols, 2022
  • A roadmap for the characterization of energy metabolism in human cardiomyocytes derived from induced pluripotent stem cells
    Giulia Emanuelli, Anna Zoccarato, Christina M. Reumiller, Angelos Papadopoulos, Mei Chong, Sabine Rebs, Kai Betteridge, Matteo Beretta, Katrin Streckfuss-Bömeke, Ajay M. Shah
    Journal of Molecular and Cellular Cardiology, 2022
  • SLM2 Is A Novel Cardiac Splicing Factor Involved in Heart Failure due to Dilated Cardiomyopathy
    Jes-Niels Boeckel, Maximilian Möbius-Winkler, Marion Müller, Sabine Rebs, Nicole Eger, Laura Schoppe, Rewati Tappu, Karoline E. Kokot, Jasmin M. Kneuer, Susanne Gaul, Diana M. Bordalo, Alan Lai, Jan Haas, Mahsa Ghanbari, Philipp Drewe-Boss, Martin Liss, Hugo A. Katus, Uwe Ohler, Michael Gotthardt, Ulrich Laufs, Katrin Streckfuss-Bömeke, Benjamin Meder
    Genomics Proteomics and Bioinformatics, 2022
  • Cardiomyocyte protein O-GlcNAcylation is regulated by GFAT1 not GFAT2
    Adam A Nabeebaccus, Sharwari Verma, Anna Zoccarato, Giulia Emanuelli, Celio XC. Santos, Katrin Streckfuss-Bömeke, Ajay M. Shah
    Biochemical and Biophysical Research Communications, 2021
  • Identification of SCN5a p.C335R variant in a large family with dilated cardiomyopathy and conduction disease
    Farbod Sedaghat-Hamedani, Sabine Rebs, Ibrahim El-Battrawy, Safak Chasan, Tobias Krause, Jan Haas, Rujia Zhong, Zhenxing Liao, Qiang Xu, Xiaobo Zhou, Ibrahim Akin, Edgar Zitron, Norbert Frey, Katrin Streckfuss-Bömeke, Elham Kayvanpour
    International Journal of Molecular Sciences, 2021
  • Detrimental proarrhythmogenic interaction of Ca2+/calmodulin-dependent protein kinase II and NaV1.8 in heart failure
    Philipp Bengel, Nataliya Dybkova, Petros Tirilomis, Shakil Ahmad, Nico Hartmann, Belal A. Mohamed, Miriam Celine Krekeler, Wiebke Maurer, Steffen Pabel, Maximilian Trum, Julian Mustroph, Jan Gummert, Hendrik Milting, Stefan Wagner, Senka Ljubojevic-Holzer, Karl Toischer, Lars S. Maier, Gerd Hasenfuss, Katrin Streckfuss-Bömeke, Samuel Sossalla
    Nature Communications, 2021
  • Truncated titin proteins and titin haploinsufficiency are targets for functional recovery in human cardiomyopathy due to TTN mutations
    Andrey Fomin, Anna Gärtner, Lukas Cyganek, Malte Tiburcy, Izabela Tuleta, Luisa Wellers, Lina Folsche, Anastasia J. Hobbach, Marion von Frieling-Salewsky, Andreas Unger, Anna Hucke, Franziska Koser, Astrid Kassner, Katharina Sielemann, Katrin Streckfuß-Bömeke, Gerd Hasenfuss, Alexander Goedel, Karl-Ludwig Laugwitz, Alessandra Moretti, Jan F. Gummert, Cristobal G. dos Remedios, Holger Reinecke, Ralph Knöll, Sebastiaan van Heesch, Norbert Hubner, Wolfram H. Zimmermann, Hendrik Milting, Wolfgang A. Linke
    Science Translational Medicine, 2021
  • Peroxisomes contribute to intracellular calcium dynamics in cardiomyocytes and non-excitable cells
    Yelena Sargsyan, Uta Bickmeyer, Christine S Gibhardt, Katrin Streckfuss-Bömeke, Ivan Bogeski, Sven Thoms
    Life Science Alliance, 2021
  • Generation and cardiac differentiation of an induced pluripotent stem cell line from a patient with arrhythmia-induced cardiomyopathy
    Sabine Rebs, Jakob Beier, Loukas Argyriou, Tillmann Schill, Gerd Hasenfuss, Dirk Vollmann, Samuel Sossalla, Katrin Streckfuss-Bömeke
    Stem Cell Research, 2021
  • Telomerase therapy attenuates cardiotoxic effects of doxorubicin
    Shambhabi Chatterjee, Teresa Hofer, Alessia Costa, Dongchao Lu, Sandor Batkai, Shashi Kumar Gupta, Emiliano Bolesani, Robert Zweigerdt, Diego Megias, Katrin Streckfuss-Bömeke, Christina Brandenberger, Thomas Thum, Christian Bär
    Molecular Therapy, 2021
  • Pluripotent stem cell‐derived mesenchymal stem cells show comparable functionality to their autologous origin
    Mark Jakob, Mario Hambrecht, Jennifer L. Spiegel, Julia Kitz, Martin Canis, Ralf Dressel, Katrin Streckfuss-Bömeke
    Cells, 2021
  • Long-term effects of empagliflozin on excitation-contraction-coupling in human induced pluripotent stem cell cardiomyocytes
    Steffen Pabel, Florian Reetz, Nataliya Dybkova, Orr Shomroni, Gabriela Salinas, Julian Mustroph, Karin P. Hammer, Gerd Hasenfuss, Nazha Hamdani, Lars S. Maier, Katrin Streckfuss-Bömeke, Samuel Sossalla
    Journal of Molecular Medicine, 2020
  • Nox4 regulates InsP3 receptor-dependent Ca2+ release into mitochondria to promote cell survival
    Matteo Beretta, Celio XC Santos, Chris Molenaar, Anne D Hafstad, Chris CJ Miller, Aram Revazian, Kai Betteridge, Katrin Schröder, Katrin Streckfuß‐Bömeke, James H Doroshow, Roland A Fleck, Tsung‐Ping Su, Vsevolod V Belousov, Maddy Parsons, Ajay M Shah
    EMBO Journal, 2020
  • High-throughput analysis for the identification of viral infections in ps-iPSCs
    Daniela Hübscher, Katrin Streckfuss-Bömeke
    Biospektrum, 2020
  • Generation of pluripotent stem cell lines and CRISPR/Cas9 modified isogenic controls from a patient with dilated cardiomyopathy harboring a RBM20 p.R634W mutation
    Sabine Rebs, Farbod Sedaghat-Hamedani, Elham Kayvanpour, Benjamin Meder, Katrin Streckfuss-Bömeke
    Stem Cell Research, 2020
  • Dysferlin links excitation-contraction coupling to structure and maintenance of the cardiac transverse-axial tubule system
    Julia Hofhuis, Kristina Bersch, Stefan Wagner, Cristina Molina, Funsho E Fakuade, Lavanya M Iyer, Katrin Streckfuss-Bömeke, Karl Toischer, Laura C Zelarayán, Niels Voigt, Viacheslav O Nikolaev, Lars S Maier, Lars Klinge, Sven Thoms
    Europace, 2020
  • Non-Human Primate iPSC Generation, Cultivation, and Cardiac Differentiation under Chemically Defined Conditions
    Michael Stauske, Ignacio Rodriguez Polo, Wadim Haas, Debbra Yasemin Knorr, Thomas Borchert, Katrin Streckfuss-Bömeke, Ralf Dressel, Iris Bartels, Malte Tiburcy, Wolfram-Hubertus Zimmermann, Rüdiger Behr
    Cells, 2020
  • CRISPLD1: a novel conserved target in the transition to human heart failure
    Sara Khadjeh, Vanessa Hindmarsh, Frederike Weber, Lukas Cyganek, Ramon O. Vidal, Setare Torkieh, Katrin Streckfuss-Bömeke, Dawid Lbik, Malte Tiburcy, Belal A. Mohamed, Stefan Bonn, Karl Toischer, Gerd Hasenfuss
    Basic Research in Cardiology, 2020
  • Generation of iPSC-lines from two independent Takotsubo syndrome patients with recurrent Takotsubo events
    Daniela Hübscher, Sabine Rebs, Wiebke Maurer, Jelena R. Ghadri, Ralf Dressel, Christian Templin, Katrin Streckfuss-Bömeke
    Stem Cell Research, 2020
  • Inhibition of NaV1.8 prevents atrial arrhythmogenesis in human and mice
    Steffen Pabel, Shakil Ahmad, Petros Tirilomis, Thea Stehle, Julian Mustroph, Maria Knierim, Nataliya Dybkova, Philipp Bengel, Andreas Holzamer, Michael Hilker, Katrin Streckfuss-Bömeke, Gerd Hasenfuss, Lars S. Maier, Samuel Sossalla
    Basic Research in Cardiology, 2020
  • Radiation-induced sensitivity of tissue-resident mesenchymal stem cells in the head and neck region
    Jennifer L. Spiegel, Mario Hambrecht, Vera Kohlbauer, Frank Haubner, Friedrich Ihler, Martin Canis, Arndt F. Schilling, Kai O. Böker, Ralf Dressel, Katrin Streckfuss‐Bömeke, Mark Jakob
    Head and Neck, 2019
  • The functional consequences of sodium channel NaV1.8 in human left ventricular hypertrophy
    Shakil Ahmad, Petros Tirilomis, Steffen Pabel, Nataliya Dybkova, Nico Hartmann, Cristina E. Molina, Theodoros Tirilomis, Ingo Kutschka, Norbert Frey, Lars S. Maier, Gerd Hasenfuss, Katrin Streckfuss-Bömeke, Samuel Sossalla
    Esc Heart Failure, 2019
  • miR-212/132 Cluster Modulation Prevents Doxorubicin-Mediated Atrophy and Cardiotoxicity
    Shashi Kumar Gupta, Ankita Garg, Petros Avramopoulos, Stefan Engelhardt, Katrin Streckfuss-Bömeke, Sandor Batkai, Thomas Thum
    Molecular Therapy, 2019
  • A high-throughput method as a diagnostic tool for HIV detection in patient-specific induced pluripotent stem cells generated by different reprogramming methods
    Daniela Hübscher, Sabine Rebs, Luis Haupt, Thomas Borchert, Celina Isabell Guessoum, Franziska Treu, Steffen Köhne, Andreas Maus, Mario Hambrecht, Samuel Sossalla, Ralf Dressel, Angela Uy, Mark Jakob, Gerd Hasenfuss, Katrin Streckfuss-Bömeke
    Stem Cells International, 2019
  • Empagliflozin directly improves diastolic function in human heart failure
    Steffen Pabel, Stefan Wagner, Hannah Bollenberg, Philipp Bengel, Árpád Kovács, Christian Schach, Petros Tirilomis, Julian Mustroph, André Renner, Jan Gummert, Thomas Fischer, Sophie Van Linthout, Carsten Tschöpe, Katrin Streckfuss-Bömeke, Gerd Hasenfuss, Lars S. Maier, Nazha Hamdani, Samuel Sossalla
    European Journal of Heart Failure, 2018
  • Differential regulation of sodium channels as a novel proarrhythmic mechanism in the human failing heart
    Nataliya Dybkova, Shakil Ahmad, Steffen Pabel, Petros Tirilomis, Nico Hartmann, Thomas H Fischer, Philipp Bengel, Theodoros Tirilomis, Senka Ljubojevic, André Renner, Jan Gummert, David Ellenberger, Stefan Wagner, Norbert Frey, Lars S Maier, Katrin Streckfuss-Bömeke, Gerd Hasenfuss, Samuel Sossalla
    Cardiovascular Research, 2018
  • Clinical nuclear medicine tracers: Easy metabolic assays in stem cell research and cardiac disease?
    Katrin Streckfuss-Bömeke
    International Journal of Cardiology, 2018
  • Clinical genetics and outcome of left ventricular non-compaction cardiomyopathy
    Farbod Sedaghat-Hamedani, Jan Haas, Feng Zhu, Christian Geier, Elham Kayvanpour, Martin Liss, Alan Lai, Karen Frese, Regina Pribe-Wolferts, Ali Amr, Daniel Tian Li, Omid Shirvani Samani, Avisha Carstensen, Diana Martins Bordalo, Marion Müller, Christine Fischer, Jing Shao, Jing Wang, Ming Nie, Li Yuan, Sabine Haßfeld, Christine Schwartz, Min Zhou, Zihua Zhou, Yanwen Shu, Min Wang, Kai Huang, Qiutang Zeng, Longxian Cheng, Tobias Fehlmann, Philipp Ehlermann, Andreas Keller, Christoph Dieterich, Katrin Streckfuß-Bömeke, Yuhua Liao, Michael Gotthardt, Hugo A Katus, Benjamin Meder
    European Heart Journal, 2017
  • Severe DCM phenotype of patient harboring RBM20 mutation S635A can be modeled by patient-specific induced pluripotent stem cell-derived cardiomyocytes
    Katrin Streckfuss-Bömeke, Malte Tiburcy, Andrey Fomin, Xiaojing Luo, Wener Li, Claudia Fischer, Cemil Özcelik, Andreas Perrot, Samuel Sossalla, Jan Haas, Ramon Oliveira Vidal, Sabine Rebs, Sara Khadjeh, Benjamin Meder, Stefan Bonn, Wolfgang A. Linke, Wolfram-Hubertus Zimmermann, Gerd Hasenfuss, Kaomei Guan
    Journal of Molecular and Cellular Cardiology, 2017
  • Catecholamine-Dependent β-Adrenergic Signaling in a Pluripotent Stem Cell Model of Takotsubo Cardiomyopathy
    Thomas Borchert, Daniela Hübscher, Celina I. Guessoum, Tuan-Dinh D. Lam, Jelena R. Ghadri, Isabel N. Schellinger, Malte Tiburcy, Norman Y. Liaw, Yun Li, Jan Haas, Samuel Sossalla, Mia A. Huber, Lukas Cyganek, Claudius Jacobshagen, Ralf Dressel, Uwe Raaz, Viacheslav O. Nikolaev, Kaomei Guan, Holger Thiele, Benjamin Meder, Bernd Wollnik, Wolfram-Hubertus Zimmermann, Thomas F. Lüscher, Gerd Hasenfuss, Christian Templin, Katrin Streckfuss-Bömeke
    Journal of the American College of Cardiology, 2017
  • Generation of a KLF15 homozygous knockout human embryonic stem cell line using paired CRISPR/Cas9n, and human cardiomyocytes derivation
    Claudia Noack, Luis Peter Haupt, Wolfram-Hubertus Zimmermann, Katrin Streckfuss-Bömeke, Laura Cecilia Zelarayán
    Stem Cell Research, 2017
  • Sensing Cardiac Electrical Activity with a Cardiac Myocyte-Targeted Optogenetic Voltage Indicator
    Mei-Ling Chang Liao, Teun P. de Boer, Hiroki Mutoh, Nour Raad, Claudia Richter, Eva Wagner, Bryan R. Downie, Bernhard Unsöld, Iqra Arooj, Katrin Streckfuss-Bömeke, Stephan Döker, Stefan Luther, Kaomei Guan, Stefan Wagner, Stephan E. Lehnart, Lars S. Maier, Walter Stühmer, Erich Wettwer, Toon van Veen, Michael M. Morlock, Thomas Knöpfel, Wolfram-Hubertus Zimmermann
    Circulation Research, 2015
  • Patient-specific iPS cells and their application in heart research
    Katrin Streckfuß-Bömeke, Lukas Cyganek
    Biospektrum, 2015
  • Human induced pluripotent stem cells are targets for allogeneic and autologous natural killer (NK) cells and killing is partly mediated by the activating NK receptor DNAM-1
    Vanessa Kruse, Carina Hamann, Sebastian Monecke, Lukas Cyganek, Leslie Elsner, Daniela Hübscher, Lutz Walter, Katrin Streckfuss-Bömeke, Kaomei Guan, Ralf Dressel
    Plos One, 2015
  • Ca2+/calmodulin-dependent protein kinase II equally induces sarcoplasmic reticulum Ca2+ leak in human ischaemic and dilated cardiomyopathy
    Thomas H. Fischer, Jörg Eiringhaus, Nataliya Dybkova, Anna Förster, Jonas Herting, Astrid Kleinwächter, Senka Ljubojevic, Jan D. Schmitto, Katrin Streckfuß-Bömeke, André Renner, Jan Gummert, Gerd Hasenfuss, Lars S. Maier, Samuel Sossalla
    European Journal of Heart Failure, 2014
  • Efficient generation of hepatic cells from multipotent adult mouse germ-line stem cells using an OP9 co-culture system
    Katrin Streckfuss-Bömeke, Jörg Jende, I-Fen Cheng, Gerd Hasenfuss, Kaomei Guan
    Cellular Reprogramming, 2014
  • Comparative study of human-induced pluripotent stem cells derived from bone marrow cells, hair keratinocytes, and skin fibroblasts
    Katrin Streckfuss-Bömeke, Frieder Wolf, Azadeh Azizian, Michael Stauske, Malte Tiburcy, Stefan Wagner, Daniela Hübscher, Ralf Dressel, Simin Chen, Jörg Jende, Gerald Wulf, Verena Lorenz, Michael P. Schön, Lars S. Maier, Wolfram H. Zimmermann, Gerd Hasenfuss, Kaomei Guan
    European Heart Journal, 2013
  • Cardiolipin deficiency affects respiratory chain function and organization in an induced pluripotent stem cell model of Barth syndrome
    Jan Dudek, I-Fen Cheng, Martina Balleininger, Frédéric M. Vaz, Katrin Streckfuss-Bömeke, Daniela Hübscher, Milena Vukotic, Ronald J.A. Wanders, Peter Rehling, Kaomei Guan
    Stem Cell Research, 2013
  • A feedback circuit between transcriptional activation and self-destruction of Gcn4 separates its metabolic and morphogenic response in diploid yeasts
    Britta Herzog, Katrin Streckfuss-Bömeke, Gerhard H. Braus
    Journal of Molecular Biology, 2011
  • Pluripotent stem cells are highly susceptible targets for syngeneic, allogeneic, and xenogeneic natural killer cells
    Ralf Dressel, Jessica Nolte, Leslie Elsner, Peter Novota, Kaomei Guan, Katrin Streckfuss‐Bömeke, Gerd Hasenfuss, Rudolf Jaenisch, Wolfgang Engel
    FASEB Journal, 2010
  • Degradation of Saccharomyces cerevisiae transcription factor Gcn4 requires a C-terminal nuclear localization signal in the cyclin Pcl5
    Katrin Streckfuss-Bömeke, Florian Schulze, Britta Herzog, Eva Scholz, Gerhard H. Braus
    Eukaryotic Cell, 2009
  • Generation of functional neurons and glia from multipotent adult mouse germ-line stem cells
    Katrin Streckfuss-Bömeke, Alla Vlasov, Swen Hülsmann, Dongjiao Yin, Karim Nayernia, Wolfgang Engel, Gerd Hasenfuss, Kaomei Guan
    Stem Cell Research, 2009
  • The Saccharomyces homolog of mammalian RACK1, Cpc2/Asc1p, is required for FLO11-dependent adhesive growth and dimorphism
    Oliver Valerius, Malte Kleinschmidt, Nicole Rachfall, Florian Schulze, Sarai López Marín, Michael Hoppert, Katrin Streckfuss-Bömeke, Claudia Fischer, Gerhard H. Braus
    Molecular and Cellular Proteomics, 2007