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3. Enhanced Ca2+-Dependent SK-Channel Gating and Membrane Trafficking in Human Atrial Fibrillation

Author

Heijman, Jordi, Zhou, Xiaobo, Morotti, Stefano, Molina, Cristina E, Abu-Taha, Issam H, Tekook, Marcel, Jespersen, Thomas, Zhang, Yiqiao, Dobrev, Shokoufeh, Milting, Hendrik, Gummert, Jan, Karck, Matthias, Kamler, Markus, El-Armouche, Ali, Saljic, Arnela, Grandi, Eleonora, Nattel, Stanley, and Dobrev, Dobromir

Subjects
Medical Physiology, Biomedical and Clinical Sciences, Cardiovascular, Heart Disease, Aetiology, 5.1 Pharmaceuticals, 2.1 Biological and endogenous factors, Development of treatments and therapeutic interventions, Animals, Humans, Atrial Fibrillation, Apamin, Primaquine, Calmodulin, Heart Atria, Myocytes, Cardiac, Anti-Arrhythmia Agents, Action Potentials, Small-Conductance Calcium-Activated Potassium Channels, actinin, apamin, atrial fibrillation, atrial remodeling, calmodulin, protein phosphatase-2A, protein transport, Cardiorespiratory Medicine and Haematology, Clinical Sciences, Cardiovascular System & Hematology, Cardiovascular medicine and haematology, Clinical sciences
Abstract

BackgroundSmall-conductance Ca2+-activated K+ (SK)-channel inhibitors have antiarrhythmic effects in animal models of atrial fibrillation (AF), presenting a potential novel antiarrhythmic option. However, the regulation of SK-channels in human atrial cardiomyocytes and its modification in patients with AF are poorly understood and were the object of this study.MethodsApamin-sensitive SK-channel current (ISK) and action potentials were recorded in human right-atrial cardiomyocytes from sinus rhythm control (Ctl) patients or patients with (long-standing persistent) chronic AF (cAF).ResultsISK was significantly higher, and apamin caused larger action potential prolongation in cAF- versus Ctl-cardiomyocytes. Sensitivity analyses in an in silico human atrial cardiomyocyte model identified IK1 and ISK as major regulators of repolarization. Increased ISK in cAF was not associated with increases in mRNA/protein levels of SK-channel subunits in either right- or left-atrial tissue homogenates or right-atrial cardiomyocytes, but the abundance of SK2 at the sarcolemma was larger in cAF versus Ctl in both tissue-slices and cardiomyocytes. Latrunculin-A and primaquine (anterograde and retrograde protein-trafficking inhibitors) eliminated the differences in SK2 membrane levels and ISK between Ctl- and cAF-cardiomyocytes. In addition, the phosphatase-inhibitor okadaic acid reduced ISK amplitude and abolished the difference between Ctl- and cAF-cardiomyocytes, indicating that reduced calmodulin-Thr80 phosphorylation due to increased protein phosphatase-2A levels in the SK-channel complex likely contribute to the greater ISK in cAF-cardiomyocytes. Finally, rapid electrical activation (5 Hz, 10 minutes) of Ctl-cardiomyocytes promoted SK2 membrane-localization, increased ISK and reduced action potential duration, effects greatly attenuated by apamin. Latrunculin-A or primaquine prevented the 5-Hz-induced ISK-upregulation.ConclusionsISK is upregulated in patients with cAF due to enhanced channel function, mediated by phosphatase-2A-dependent calmodulin-Thr80 dephosphorylation and tachycardia-dependent enhanced trafficking and targeting of SK-channel subunits to the sarcolemma. The observed AF-associated increases in ISK, which promote reentry-stabilizing action potential duration shortening, suggest an important role for SK-channels in AF auto-promotion and provide a rationale for pursuing the antiarrhythmic effects of SK-channel inhibition in humans.

Published
2023

6. Inflammation and vascular remodeling in COVID-19 hearts

Author

Werlein, Christopher, Ackermann, Maximilian, Stark, Helge, Shah, Harshit R., Tzankov, Alexandar, Haslbauer, Jasmin Dinonne, von Stillfried, Saskia, Bülow, Roman David, El-Armouche, Ali, Kuenzel, Stephan, Robertus, Jan Lukas, Reichardt, Marius, Haverich, Axel, Höfer, Anne, Neubert, Lavinia, Plucinski, Edith, Braubach, Peter, Verleden, Stijn, Salditt, Tim, Marx, Nikolaus, Welte, Tobias, Bauersachs, Johann, Kreipe, Hans-Heinrich, Mentzer, Steven J., Boor, Peter, Black, Stephen M., Länger, Florian, Kuehnel, Mark, and Jonigk, Danny

Published
2023
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9. Loss of CASK Accelerates Heart Failure Development

Author

Mustroph, Julian, Sag, Can M, Bähr, Felix, Schmidtmann, Anna-Lena, Gupta, Shamindra N, Dietz, Alexander, Islam, MM Towhidul, Lücht, Charlotte, Beuthner, Bo Eric, Pabel, Steffen, Baier, Maria J, El-Armouche, Ali, Sossalla, Samuel, Anderson, Mark E, Möllmann, Julia, Lehrke, Michael, Marx, Nikolaus, Mohler, Peter J, Bers, Donald M, Unsöld, Bernhard, He, Tao, Dewenter, Matthias, Backs, Johannes, Maier, Lars S, and Wagner, Stefan

Subjects
Biomedical and Clinical Sciences, Cardiovascular Medicine and Haematology, Clinical Sciences, Animals, Calcium, Calcium-Calmodulin-Dependent Protein Kinase Type 2, Cells, Cultured, Glucagon-Like Peptide-1 Receptor, Guanylate Kinases, Heart Failure, Heart Rate, Humans, Male, Mice, Mice, Inbred C57BL, Myocardial Contraction, Myocytes, Cardiac, calmodulin, heart failure, myocardium, neurons, sarcoplasmic reticulum, Cardiorespiratory Medicine and Haematology, Cardiovascular System & Hematology, Cardiovascular medicine and haematology, Clinical sciences
Abstract

[Figure: see text].

Published
2021

12. Gene therapy with phosphodiesterases 2A and 4B ameliorates heart failure and arrhythmias by improving subcellular cAMP compartmentation

Author

Pavlaki, Nikoleta, primary, Froese, Alexander, additional, Li, Wener, additional, De Jong, Kirstie A, additional, Geertz, Birgit, additional, Subramanian, Hariharan, additional, Mohagaonkar, Sanika, additional, Luo, Xiaojing, additional, Schubert, Mario, additional, Wiegmann, Robert, additional, Margaria, Jean Piero, additional, Ghigo, Alessandra, additional, Kämmerer, Susanne, additional, Hirsch, Emilio, additional, El-Armouche, Ali, additional, Guan, Kaomei, additional, and Nikolaev, Viacheslav O, additional

Published
2024
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14. Targeting cardiomyocyte ADAM10 ectodomain shedding promotes survival early after myocardial infarction

Author

Klapproth, Erik, Witt, Anke, Klose, Pauline, Wiedemann, Johanna, Vavilthota, Nikitha, Künzel, Stephan R., Kämmerer, Susanne, Günscht, Mario, Sprott, David, Lesche, Mathias, Rost, Fabian, Dahl, Andreas, Rauch, Erik, Kattner, Lars, Weber, Silvio, Mirtschink, Peter, Kopaliani, Irakli, Guan, Kaomei, Lorenz, Kristina, Saftig, Paul, Wagner, Michael, and El-Armouche, Ali

Published
2022
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15. Skeletal muscle derived Musclin protects the heart during pathological overload

Author

Szaroszyk, Malgorzata, Kattih, Badder, Martin-Garrido, Abel, Trogisch, Felix A., Dittrich, Gesine M., Grund, Andrea, Abouissa, Aya, Derlin, Katja, Meier, Martin, Holler, Tim, Korf-Klingebiel, Mortimer, Völker, Katharina, Garfias Macedo, Tania, Pablo Tortola, Cristina, Boschmann, Michael, Huang, Nora, Froese, Natali, Zwadlo, Carolin, Malek Mohammadi, Mona, Luo, Xiaojing, Wagner, Michael, Cordero, Julio, Geffers, Robert, Batkai, Sandor, Thum, Thomas, Bork, Nadja, Nikolaev, Viacheslav O., Müller, Oliver J., Katus, Hugo A., El-Armouche, Ali, Kraft, Theresia, Springer, Jochen, Dobreva, Gergana, Wollert, Kai C., Fielitz, Jens, von Haehling, Stephan, Kuhn, Michaela, Bauersachs, Johann, and Heineke, Joerg

Published
2022
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16. CNP Promotes Antiarrhythmic Effects via Phosphodiesterase 2

Author

Cachorro, Eleder, Günscht, Mario, Schubert, Mario, Sadek, Mirna S., Siegert, Johanna, Dutt, Fabian, Bauermeister, Carla, Quickert, Susann, Berning, Henrick, Nowakowski, Felix, Lämmle, Simon, Firneburg, Rebecca, Luo, Xiaojing, Künzel, Stephan R., Klapproth, Erik, Mirtschink, Peter, Mayr, Manuel, Dewenter, Matthias, Vettel, Christiane, Heijman, Jordi, Lorenz, Kristina, Guan, Kaomei, El-Armouche, Ali, Wagner, Michael, and Kämmerer, Susanne

Published
2023
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17. Comprehensive promotion of iPSC-CM maturation by integrating metabolic medium, nanopatterning, and electrostimulation

Author

Guan, Kaomei, primary, Li, Wener, additional, Luo, Xiaojing, additional, Strano, Anna, additional, Arun, Shakthi, additional, Gamm, Oliver, additional, Pötsch, Mareike, additional, Hasse, Marcel, additional, Steiner, Robert, additional, Fischer, Konstanze, additional, Pöche, Jessie, additional, Ulbricht, Ying, additional, Lesche, Mathias, additional, Trimaglio, Giulia, additional, El-Armouche, Ali, additional, Dahl, Andreas, additional, Mirtschink, Peter, additional, and Schubert, Mario, additional

Published
2024
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19. Calcium/Calmodulin-Dependent Protein Kinase II Activity Persists During Chronic &bgr;-Adrenoceptor Blockade in Experimental and Human Heart Failure

Author

Dewenter, Matthias, Neef, Stefan, Vettel, Christiane, Lämmle, Simon, Beushausen, Christina, Zelarayan, Laura C, Katz, Sylvia, von der Lieth, Albert, Meyer-Roxlau, Stefanie, Weber, Silvio, Wieland, Thomas, Sossalla, Samuel, Backs, Johannes, Brown, Joan H, Maier, Lars S, and El-Armouche, Ali

Subjects
Medical Physiology, Biomedical and Clinical Sciences, Heart Disease, Cardiovascular, Aetiology, Development of treatments and therapeutic interventions, 2.1 Biological and endogenous factors, 5.1 Pharmaceuticals, Adrenergic beta-Antagonists, Animals, Calcium-Calmodulin-Dependent Protein Kinase Type 2, Disease Models, Animal, Echocardiography, Heart Failure, Humans, Immunoblotting, Metoprolol, Mice, Mice, Transgenic, beta-adrenergic blockers, calcium, calmodulin-dependent protein kinase type 2, heart failure, calcium/calmodulin-dependent protein kinase type 2, Biochemistry and Cell Biology, Cardiorespiratory Medicine and Haematology, Cardiovascular System & Hematology, Cardiovascular medicine and haematology, Medical physiology
Abstract

BackgroundConsiderable evidence suggests that calcium/calmodulin-dependent protein kinase II (CaMKII) overactivity plays a crucial role in the pathophysiology of heart failure (HF), a condition characterized by excessive β-adrenoceptor (β-AR) stimulation. Recent studies indicate a significant cross talk between β-AR signaling and CaMKII activation presenting CaMKII as a possible downstream mediator of detrimental β-AR signaling in HF. In this study, we investigated the effect of chronic β-AR blocker treatment on CaMKII activity in human and experimental HF.Methods and resultsImmunoblot analysis of myocardium from end-stage HF patients (n=12) and non-HF subjects undergoing cardiac surgery (n=12) treated with β-AR blockers revealed no difference in CaMKII activity when compared with non-β-AR blocker-treated patients. CaMKII activity was judged by analysis of CaMKII expression, autophosphorylation, and oxidation and by investigating the phosphorylation status of CaMKII downstream targets. To further evaluate these findings, CaMKIIδC transgenic mice were treated with the β1-AR blocker metoprolol (270 mg/kg*d). Metoprolol significantly reduced transgene-associated mortality (n≥29; P

Published
2017

20. Calcium/Calmodulin-Dependent Protein Kinase II Activity Persists During Chronic β-Adrenoceptor Blockade in Experimental and Human Heart Failure.

Author

Dewenter, Matthias, Neef, Stefan, Vettel, Christiane, Lämmle, Simon, Beushausen, Christina, Zelarayan, Laura C, Katz, Sylvia, von der Lieth, Albert, Meyer-Roxlau, Stefanie, Weber, Silvio, Wieland, Thomas, Sossalla, Samuel, Backs, Johannes, Brown, Joan H, Maier, Lars S, and El-Armouche, Ali

Subjects
Animals, Mice, Transgenic, Humans, Mice, Disease Models, Animal, Metoprolol, Adrenergic beta-Antagonists, Echocardiography, Immunoblotting, Heart Failure, Calcium-Calmodulin-Dependent Protein Kinase Type 2, beta-adrenergic blockers, calcium/calmodulin-dependent protein kinase type 2, heart failure, calcium, calmodulin-dependent protein kinase type 2, Transgenic, Disease Models, Animal, Cardiovascular System & Hematology, Biochemistry and Cell Biology, Cardiorespiratory Medicine and Haematology, Medical Physiology
Abstract

BackgroundConsiderable evidence suggests that calcium/calmodulin-dependent protein kinase II (CaMKII) overactivity plays a crucial role in the pathophysiology of heart failure (HF), a condition characterized by excessive β-adrenoceptor (β-AR) stimulation. Recent studies indicate a significant cross talk between β-AR signaling and CaMKII activation presenting CaMKII as a possible downstream mediator of detrimental β-AR signaling in HF. In this study, we investigated the effect of chronic β-AR blocker treatment on CaMKII activity in human and experimental HF.Methods and resultsImmunoblot analysis of myocardium from end-stage HF patients (n=12) and non-HF subjects undergoing cardiac surgery (n=12) treated with β-AR blockers revealed no difference in CaMKII activity when compared with non-β-AR blocker-treated patients. CaMKII activity was judged by analysis of CaMKII expression, autophosphorylation, and oxidation and by investigating the phosphorylation status of CaMKII downstream targets. To further evaluate these findings, CaMKIIδC transgenic mice were treated with the β1-AR blocker metoprolol (270 mg/kg*d). Metoprolol significantly reduced transgene-associated mortality (n≥29; P

Published
2017

21. HIF1α is a direct regulator of steroidogenesis in the adrenal gland

Author

Watts, Deepika, Stein, Johanna, Meneses, Ana, Bechmann, Nicole, Neuwirth, Ales, Kaden, Denise, Krüger, Anja, Sinha, Anupam, Alexaki, Vasileia Ismini, Luis Gustavo Perez-Rivas, Kircher, Stefan, Martinez, Antoine, Theodoropoulou, Marily, Eisenhofer, Graeme, Peitzsch, Mirko, El-Armouche, Ali, Chavakis, Triantafyllos, and Wielockx, Ben

Published
2021
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23. Antithrombotische Therapie nach strukturellen kardialen Interventionen: Empfehlung der Arbeitsgruppe Kardiovaskuläre Hämostase und Antithrombotische Therapie (AG19) der Deutschen Gesellschaft für Kardiologie – Herz- und Kreislaufforschung e. V. (DGK) in Zusammenarbeit mit der Arbeitsgruppe Interventionelle Kardiologie (AG6) – AGIK und der Arbeitsgruppe Klinische Pharmakologie (AG22) der DGK

Author

Hochholzer, Willibald, Nührenberg, Thomas, Flierl, Ulrike, Olivier, Christoph B., Landmesser, Ulf, Möllmann, Helge, Dörr, Marcus, Mehilli, Julinda, Schäfer, Andreas, Dürschmied, Daniel, Sibbing, Dirk, El-Armouche, Ali, Zeymer, Uwe, Neumann, Franz-Josef, Ahrens, Ingo, and Geisler, Tobias

Published
2021
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25. Control of cytoplasmic and nuclear protein kinase A by phosphodiesterases and phosphatases in cardiac myocytes

Author

Slimane, Zeineb Haj, Bedioune, Ibrahim, Lechêne, Patrick, Varin, Audrey, Lefebvre, Florence, Mateo, Philippe, Domergue-Dupont, Valérie, Dewenter, Matthias, Richter, Wito, Conti, Marco, El-Armouche, Ali, Zhang, Jin, Fischmeister, Rodolphe, and Vandecasteele, Grégoire

Subjects
Medical Physiology, Biomedical and Clinical Sciences, Heart Disease, Cardiovascular, 1.1 Normal biological development and functioning, 2.1 Biological and endogenous factors, Underpinning research, Aetiology, Animals, Cardiotonic Agents, Cell Nucleus, Cyclic AMP, Cyclic AMP Response Element-Binding Protein, Cyclic AMP-Dependent Protein Kinases, Cytoplasm, Isoproterenol, Male, Myocytes, Cardiac, Nuclear Proteins, Phosphodiesterase Inhibitors, Phosphoric Diester Hydrolases, Phosphoric Monoester Hydrolases, Phosphorylation, Rats, Wistar, Receptors, Adrenergic, Signal Transduction, cAMP-dependent protein kinase, Compartmentation, 3'-5'-cyclic nucleotide phosphodiesterases, Ser/Thr protein phosphatases, Nucleus, 3′–5′-cyclic nucleotide phosphodiesterases, Cardiorespiratory Medicine and Haematology, Cardiovascular System & Hematology, Cardiovascular medicine and haematology
Abstract

AimsThe cAMP-dependent protein kinase (PKA) mediates β-adrenoceptor (β-AR) regulation of cardiac contraction and gene expression. Whereas PKA activity is well characterized in various subcellular compartments of adult cardiomyocytes, its regulation in the nucleus remains largely unknown. The aim of the present study was to compare the modalities of PKA regulation in the cytoplasm and nucleus of cardiomyocytes.Methods and resultsCytoplasmic and nuclear cAMP and PKA activity were measured with targeted fluorescence resonance energy transfer probes in adult rat ventricular myocytes. β-AR stimulation with isoprenaline (Iso) led to fast cAMP elevation in both compartments, whereas PKA activity was fast in the cytoplasm but markedly slower in the nucleus. Iso was also more potent and efficient in activating cytoplasmic than nuclear PKA. Similar slow kinetics of nuclear PKA activation was observed upon adenylyl cyclase activation with L-858051 or phosphodiesterase (PDE) inhibition with 3-isobutyl-1-methylxantine. Consistently, pulse stimulation with Iso (15 s) maximally induced PKA and myosin-binding protein C phosphorylation in the cytoplasm, but marginally activated PKA and cAMP response element-binding protein phosphorylation in the nucleus. Inhibition of PDE4 or ablation of the Pde4d gene in mice prolonged cytoplasmic PKA activation and enhanced nuclear PKA responses. In the cytoplasm, phosphatase 1 (PP1) and 2A (PP2A) contributed to the termination of PKA responses, whereas only PP1 played a role in the nucleus.ConclusionOur study reveals a differential integration of cytoplasmic and nuclear PKA responses to β-AR stimulation in cardiac myocytes. This may have important implications in the physiological and pathological hypertrophic response to β-AR stimulation.

Published
2014

30. Nitro-fatty acids suppress ischemic ventricular arrhythmias by preserving calcium homeostasis

Author

Mollenhauer, Martin, Mehrkens, Dennis, Klinke, Anna, Lange, Max, Remane, Lisa, Friedrichs, Kai, Braumann, Simon, Geißen, Simon, Simsekyilmaz, Sakine, Nettersheim, Felix S., Lee, Samuel, Peinkofer, Gabriel, Geisler, Anne C., Geis, Bianca, Schwoerer, Alexander P., Carrier, Lucie, Freeman, Bruce A., Dewenter, Matthias, Luo, Xiaojing, El-Armouche, Ali, Wagner, Michael, Adam, Matti, Baldus, Stephan, and Rudolph, Volker

Published
2020
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31. Interference with ERK-dimerization at the nucleocytosolic interface targets pathological ERK1/2 signaling without cardiotoxic side-effects

Author

Tomasovic, Angela, Brand, Theresa, Schanbacher, Constanze, Kramer, Sofia, Hümmert, Martin W., Godoy, Patricio, Schmidt-Heck, Wolfgang, Nordbeck, Peter, Ludwig, Jonas, Homann, Susanne, Wiegering, Armin, Shaykhutdinov, Timur, Kratz, Christoph, Knüchel, Ruth, Müller-Hermelink, Hans-Konrad, Rosenwald, Andreas, Frey, Norbert, Eichler, Jutta, Dobrev, Dobromir, El-Armouche, Ali, Hengstler, Jan G., Müller, Oliver J., Hinrichs, Karsten, Cuello, Friederike, Zernecke, Alma, and Lorenz, Kristina

Published
2020
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34. A proteolytic fragment of histone deacetylase 4 protects the heart from failure by regulating the hexosamine biosynthetic pathway

Author

Lehmann, Lorenz H, Jebessa, Zegeye H, Kreusser, Michael M, Horsch, Axel, He, Tao, Kronlage, Mariya, Dewenter, Matthias, Sramek, Viviana, Oehl, Ulrike, Krebs-Haupenthal, Jutta, von der Lieth, Albert H, Schmidt, Andrea, Sun, Qiang, Ritterhoff, Julia, Finke, Daniel, Völkers, Mirko, Jungmann, Andreas, Sauer, Sven W, Thiel, Christian, Nickel, Alexander, Kohlhaas, Michael, Schäfer, Michaela, Sticht, Carsten, Maack, Christoph, Gretz, Norbert, Wagner, Michael, El-Armouche, Ali, Maier, Lars S, Londoño, Juan E Camacho, Meder, Benjamin, Freichel, Marc, Gröne, Hermann-Josef, Most, Patrick, Müller, Oliver J, Herzig, Stephan, Furlong, Eileen E M, Katus, Hugo A, and Backs, Johannes

Subjects
Heart failure -- Prevention -- Research, Quantitative trait loci -- Research, Gene expression -- Research, Histones -- Physiological aspects -- Research, Biological sciences, Health
Abstract

The stress-responsive epigenetic repressor histone deacetylase 4 (HDAC4) regulates cardiac gene expression. Here we show that the levels of an N-terminal proteolytically derived fragment of HDAC4, termed HDAC4-NT, are lower in failing mouse hearts than in healthy control hearts. Virus-mediated transfer of the portion of the Hdac4 gene encoding HDAC4-NT into the mouse myocardium protected the heart from remodeling and failure; this was associated with decreased expression of Nr4a1, which encodes a nuclear orphan receptor, and decreased NR4A1-dependent activation of the hexosamine biosynthetic pathway (HBP). Conversely, exercise enhanced HDAC4-NT levels, and mice with a cardiomyocyte-specific deletion of Hdac4 show reduced exercise capacity, which was characterized by cardiac fatigue and increased expression of Nr4a1. Mechanistically, we found that NR4A1 negatively regulated contractile function in a manner that depended on the HBP and the calcium sensor STIM1. Our work describes a new regulatory axis in which epigenetic regulation of a metabolic pathway affects calcium handling. Activation of this axis during intermittent physiological stress promotes cardiac function, whereas its impairment in sustained pathological cardiac stress leads to heart failure., Author(s): Lorenz H Lehmann [1, 2, 3]; Zegeye H Jebessa [1, 2]; Michael M Kreusser [1, 2, 3]; Axel Horsch [1, 2]; Tao He [1, 2]; Mariya Kronlage [1, 2, [...]

Published
2018
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35. Enhanced Ca 2+ -Dependent SK-Channel Gating and Membrane Trafficking in Human Atrial Fibrillation

Author

Heijman, Jordi, primary, Zhou, Xiaobo, additional, Morotti, Stefano, additional, Molina, Cristina E., additional, Abu-Taha, Issam H., additional, Tekook, Marcel, additional, Jespersen, Thomas, additional, Zhang, Yiqiao, additional, Dobrev, Shokoufeh, additional, Milting, Hendrik, additional, Gummert, Jan, additional, Karck, Matthias, additional, Kamler, Markus, additional, El-Armouche, Ali, additional, Saljic, Arnela, additional, Grandi, Eleonora, additional, Nattel, Stanley, additional, and Dobrev, Dobromir, additional

Published
2023
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36. Clinician scientists in cardiovascular medicine Position paper of the German Cardiac Society

Author

Hilgendorf, Ingo, Backs, Johannes, Baldus, Stephan, Chen, Jessy, Duncker, David, El-Armouche, Ali, Frey, Norbert, Hilfiker-Kleiner, Denise, Johnson, Victoria, Kuenzel, Stephan, Wollert, Kai C., Zeiher, Andreas, Sager, Hendrik B., Hilgendorf, Ingo, Backs, Johannes, Baldus, Stephan, Chen, Jessy, Duncker, David, El-Armouche, Ali, Frey, Norbert, Hilfiker-Kleiner, Denise, Johnson, Victoria, Kuenzel, Stephan, Wollert, Kai C., Zeiher, Andreas, and Sager, Hendrik B.

Abstract

Policy makers in academic medicine, the educational and research sectors, and industry all agree: clinician scientists, physicians engaged in research, are the key to translating and implementing innovative therapeutic concepts into clinical practice. To this end, research on cardiovascular diseases, which cause most cases of death in the world, must be prioritized. Following internal group discussions and surveying physicians working in university hospitals and affiliated research institutes, the German Cardiac Society thoroughly analyzed the current and future situation and role of clinician scientists in cardiovascular medicine. Modern cardiology at university hospitals is characterized by higher workloads with more patients, shorter hospital stays, and increasingly more complex interventions, making it difficult for physicians and department heads to combine their research interests and activities with their clinical duties and training. This position paper discusses possibilities to improve working conditions and career perspectives for clinician scientists in cardiovascular medicine.

Published
2023

38. Investigation of mesalazine as an antifibrotic drug following myocardial infarction in male mice.

Author

Künzel, Stephan R., Winter, Luise, Hoffmann, Maximilian, Kant, Theresa A., Thiel, Jessica, Kronstein‐Wiedemann, Romy, Klapproth, Erik, Lorenz, Kristina, El‐Armouche, Ali, and Kämmerer, Susanne

Subjects
MYOCARDIAL infarction, MESALAMINE, HEART fibrosis, MYOCARDIUM, HEART diseases
Abstract

Objectives: Myocardial infarction (MI) initiates a complex reparative response during which damaged cardiac muscle is replaced by connective tissue. While the initial repair is essential for survival, excessive fibrosis post‐MI is a primary contributor to progressive cardiac dysfunction, and ultimately heart failure. Currently, there are no approved drugs for the prevention or the reversal of cardiac fibrosis. Therefore, we tested the therapeutic potential of repurposed mesalazine as a post‐MI therapy, as distinct antifibrotic effects have recently been demonstrated. Methods: At 8 weeks of age, MI was induced in male C57BL/6J mice by LAD ligation. Mesalazine was administered orally at a dose of 100 μg/g body weight in drinking water. Fluid intake, weight development, and cardiac function were monitored for 28 days post intervention. Fibrosis parameters were assessed histologically and via qPCR. Results: Compared to controls, mesalazine treatment offered no survival benefit. However, no adverse effects on heart and kidney function and weight development were observed, either. While total cardiac fibrosis remained largely unaffected by mesalazine treatment, we found a distinct reduction of perivascular fibrosis alongside reduced cardiac collagen expression. Conclusions: Our findings warrant further studies on mesalazine as a potential add‐on therapy post‐MI, as perivascular fibrosis development was successfully prevented. [ABSTRACT FROM AUTHOR]

Published
2023
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41. Clinician Scientists in der kardiovaskulären Medizin

Author

Hilgendorf, Ingo, primary, Backs, Johannes, additional, Baldus, Stephan, additional, Chen, Jessy, additional, Duncker, David, additional, El-Armouche, Ali, additional, Frey, Norbert, additional, Hilfiker-Kleiner, Denise, additional, Johnson, Victoria, additional, Künzel, Stephan, additional, Wollert, Kai C., additional, Zeiher, Andreas, additional, and Sager, Hendrik B., additional

Published
2022
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43. Inflammation and vascular remodeling in COVID-19 hearts

Author

Werlein, Christopher, primary, Ackermann, Maximilian, additional, Stark, Helge, additional, Shah, Harshit R., additional, Tzankov, Alexandar, additional, Haslbauer, Jasmin Dinonne, additional, von Stillfried, Saskia, additional, Bülow, Roman David, additional, El-Armouche, Ali, additional, Kuenzel, Stephan, additional, Robertus, Jan Lukas, additional, Reichardt, Marius, additional, Haverich, Axel, additional, Höfer, Anne, additional, Neubert, Lavinia, additional, Plucinski, Edith, additional, Braubach, Peter, additional, Verleden, Stijn, additional, Salditt, Tim, additional, Marx, Nikolaus, additional, Welte, Tobias, additional, Bauersachs, Johann, additional, Kreipe, Hans-Heinrich, additional, Mentzer, Steven J., additional, Boor, Peter, additional, Black, Stephen M., additional, Länger, Florian, additional, Kuehnel, Mark, additional, and Jonigk, Danny, additional

Published
2022
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49. Phosphodiesterase-2 Is Up-Regulated in Human Failing Hearts and Blunts β-Adrenergic Responses in Cardiomyocytes

Author

Mehel, Hind, Emons, Julius, Vettel, Christiane, Wittköpper, Katrin, Seppelt, Danilo, Dewenter, Matthias, Lutz, Susanne, Sossalla, Samuel, Maier, Lars S., Lechêne, Patrick, Leroy, Jérôme, Lefebvre, Florence, Varin, Audrey, Eschenhagen, Thomas, Nattel, Stanley, Dobrev, Dobromir, Zimmermann, Wolfram-Hubertus, Nikolaev, Viacheslav O., Vandecasteele, Grégoire, Fischmeister, Rodolphe, and El-Armouche, Ali

Published
2013
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