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3. AKAP18δ Anchors and Regulates CaMKII Activity at Phospholamban-SERCA2 and RYR

Author

Carlson, Cathrine R, Aronsen, Jan Magnus, Bergan-Dahl, Anna, Moutty, Marie Christine, Lunde, Marianne, Lunde, Per Kristian, Jarstadmarken, Hilde, Wanichawan, Pimthanya, Pereira, Laetitia, Kolstad, Terje RS, Dalhus, Bjørn, Subramanian, Hariharan, Hille, Susanne, Christensen, Geir, Müller, Oliver J, Nikolaev, Viacheslav, Bers, Donald M, Sjaastad, Ivar, Shen, Xin, Louch, William E, Klussmann, Enno, and Sejersted, Ole M

Subjects
Medical Physiology, Biomedical and Clinical Sciences, Adaptor Proteins, Signal Transducing, Animals, Binding Sites, Calcium Signaling, Calcium-Binding Proteins, Calcium-Calmodulin-Dependent Protein Kinase Type 2, Cells, Cultured, HEK293 Cells, Humans, Myocytes, Cardiac, Protein Binding, Rats, Rats, Wistar, Ryanodine Receptor Calcium Release Channel, Sarcoplasmic Reticulum Calcium-Transporting ATPases, calmodulin, calcium-calmodulin-dependent protein kinase type 2, myocytes, cardiac, phospholamban, ryanodine receptor, sarcoplasmic reticulum calcium-transporting ATPases, myocytes, cardiac, Cardiorespiratory Medicine and Haematology, Clinical Sciences, Cardiovascular System & Hematology, Cardiovascular medicine and haematology, Clinical sciences
Abstract

BackgroundThe sarcoplasmic reticulum (SR) Ca2+-ATPase 2 (SERCA2) mediates Ca2+ reuptake into SR and thereby promotes cardiomyocyte relaxation, whereas the ryanodine receptor (RYR) mediates Ca2+ release from SR and triggers contraction. Ca2+/CaMKII (CaM [calmodulin]-dependent protein kinase II) regulates activities of SERCA2 through phosphorylation of PLN (phospholamban) and RYR through direct phosphorylation. However, the mechanisms for CaMKIIδ anchoring to SERCA2-PLN and RYR and its regulation by local Ca2+ signals remain elusive. The objective of this study was to investigate CaMKIIδ anchoring and regulation at SERCA2-PLN and RYR.MethodsA role for AKAP18δ (A-kinase anchoring protein 18δ) in CaMKIIδ anchoring and regulation was analyzed by bioinformatics, peptide arrays, cell-permeant peptide technology, immunoprecipitations, pull downs, transfections, immunoblotting, proximity ligation, FRET-based CaMKII activity and ELISA-based assays, whole cell and SR vesicle fluorescence imaging, high-resolution microscopy, adenovirus transduction, adenoassociated virus injection, structural modeling, surface plasmon resonance, and alpha screen technology.ResultsOur results show that AKAP18δ anchors and directly regulates CaMKIIδ activity at SERCA2-PLN and RYR, via 2 distinct AKAP18δ regions. An N-terminal region (AKAP18δ-N) inhibited CaMKIIδ through binding of a region homologous to the natural CaMKII inhibitor peptide and the Thr17-PLN region. AKAP18δ-N also bound CaM, introducing a second level of control. Conversely, AKAP18δ-C, which shares homology to neuronal CaMKIIα activator peptide (N2B-s), activated CaMKIIδ by lowering the apparent Ca2+ threshold for kinase activation and inducing CaM trapping. While AKAP18δ-C facilitated faster Ca2+ reuptake by SERCA2 and Ca2+ release through RYR, AKAP18δ-N had opposite effects. We propose a model where the 2 unique AKAP18δ regions fine-tune Ca2+-frequency-dependent activation of CaMKIIδ at SERCA2-PLN and RYR.ConclusionsAKAP18δ anchors and functionally regulates CaMKII activity at PLN-SERCA2 and RYR, indicating a crucial role of AKAP18δ in regulation of the heartbeat. To our knowledge, this is the first protein shown to enhance CaMKII activity in heart and also the first AKAP (A-kinase anchoring protein) reported to anchor a CaMKII isoform, defining AKAP18δ also as a CaM-KAP.

Published
2022

4. Therapeutic Innovations for Heart Failure

Author

Remes, Anca, Frank, Derk, Müller, Oliver J., Hecker, Markus, Editor-in-Chief, Duncker, Dirk J., Editor-in-Chief, Backs, Johannes, Series Editor, Freichel, Marc, Series Editor, Mayr, Manuel, Series Editor, Pohl, Ulrich, Series Editor, Xiao, Junjie, Series Editor, Merkus, Daphne, Series Editor, and Parker, Sarah, Series Editor

Published
2023
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5. Regnase-1 overexpression as a therapeutic approach of Marfan syndrome

Author

Noormalal, Marie, Schmiedel, Nesrin, Bozoglu, Tarik, Matzen, Andrea, Hille, Susanne, Basha, Dima Ibrahim, Vijaya Shetty, Prithviraj Manohar, Wolf, Anja, Zaradzki, Marcin, Arif, Rawa, Pühler, Thomas, Lutter, Georg, Wagner, Andreas H., Kupatt, Christian, Frank, Derk, Frey, Norbert, Remes, Anca, and Müller, Oliver J.

Published
2024
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8. Restored autophagy is protective against PAK3-induced cardiac dysfunction

Author

Ruiz-Velasco, Andrea, Raja, Rida, Chen, Xinyi, Ganenthiran, Haresh, Kaur, Namrita, Alatawi, Nasser hawimel o, Miller, Jessica M., Abouleisa, Riham R.E., Ou, Qinghui, Zhao, Xiangjun, Fonseka, Oveena, Wang, Xin, Hille, Susanne S., Frey, Norbert, Wang, Tao, Mohamed, Tamer M.A., Müller, Oliver J., Cartwright, Elizabeth J., and Liu, Wei

Published
2023
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11. A human cell atlas of the pressure-induced hypertrophic heart

Author

Nicin, Luka, Schroeter, Sam Michael, Glaser, Simone Franziska, Schulze-Brüning, Ralf, Pham, Minh-Duc, Hille, Susanne S., Yekelchyk, Michail, Kattih, Badder, Abplanalp, Wesley Tyler, Tombor, Lukas, Müller, Oliver J., Braun, Thomas, Meder, Benjamin, Reich, Christoph, Arsalan, Mani, Holubec, Tomas, Walther, Thomas, Emrich, Fabian, Krishnan, Jaya, Zeiher, Andreas M., John, David, and Dimmeler, Stefanie

Published
2022
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12. Reduction of A-to-I RNA editing in the failing human heart regulates formation of circular RNAs

Author

Kokot, Karoline E., Kneuer, Jasmin M., John, David, Rebs, Sabine, Möbius-Winkler, Maximilian N., Erbe, Stephan, Müller, Marion, Andritschke, Michael, Gaul, Susanne, Sheikh, Bilal N., Haas, Jan, Thiele, Holger, Müller, Oliver J., Hille, Susanne, Leuschner, Florian, Dimmeler, Stefanie, Streckfuss-Bömeke, Katrin, Meder, Benjamin, Laufs, Ulrich, and Boeckel, Jes-Niels

Published
2022
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14. 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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15. Kardio-Onkologie

Author

Lorenz Lehmann, Carsten Bokemeyer, Oliver J. Müller, Oliver J. Müller, Lorenz Lehmann, Carsten Bokemeyer and Lorenz Lehmann, Carsten Bokemeyer, Oliver J. Müller, Oliver J. Müller, Lorenz Lehmann, Carsten Bokemeyer

Published
2022

16. Inhibition of soluble epoxide hydrolase prevents diabetic retinopathy

Author

Hu, Jiong, Dziumbla, Sarah, Lin, Jihong, Bibli, Sofia-Iris, Zukunft, Sven, de Mos, Julian, Awwad, Khader, Frömel, Timo, Jungmann, Andreas, Devraj, Kavi, Cheng, Zhixing, Wang, Liya, Fauser, Sascha, Eberhart, Charles G, Sodhi, Akrit, Hammock, Bruce D, Liebner, Stefan, Müller, Oliver J, Glaubitz, Clemens, Hammes, Hans-Peter, Popp, Rüdiger, and Fleming, Ingrid

Subjects
Biomedical and Clinical Sciences, Ophthalmology and Optometry, Diabetes, Eye Disease and Disorders of Vision, Metabolic and endocrine, Animals, Antigens, CD, Cadherins, Capillary Permeability, Carrier Proteins, Cell Membrane, Cell Movement, Cell Survival, Diabetic Retinopathy, Disease Models, Animal, Disease Progression, Docosahexaenoic Acids, Endothelial Cells, Ependymoglial Cells, Epoxide Hydrolases, Fatty Acids, Unsaturated, Female, Humans, Intercellular Junctions, Male, Mice, Mice, Inbred C57BL, Pancreatic Elastase, Pericytes, Presenilin-1, Retina, Solubility, Vitreous Body, General Science & Technology
Abstract

Diabetic retinopathy is an important cause of blindness in adults, and is characterized by progressive loss of vascular cells and slow dissolution of inter-vascular junctions, which result in vascular leakage and retinal oedema. Later stages of the disease are characterized by inflammatory cell infiltration, tissue destruction and neovascularization. Here we identify soluble epoxide hydrolase (sEH) as a key enzyme that initiates pericyte loss and breakdown of endothelial barrier function by generating the diol 19,20-dihydroxydocosapentaenoic acid, derived from docosahexaenoic acid. The expression of sEH and the accumulation of 19,20-dihydroxydocosapentaenoic acid were increased in diabetic mouse retinas and in the retinas and vitreous humour of patients with diabetes. Mechanistically, the diol targeted the cell membrane to alter the localization of cholesterol-binding proteins, and prevented the association of presenilin 1 with N-cadherin and VE-cadherin, thereby compromising pericyte-endothelial cell interactions and inter-endothelial cell junctions. Treating diabetic mice with a specific sEH inhibitor prevented the pericyte loss and vascular permeability that are characteristic of non-proliferative diabetic retinopathy. Conversely, overexpression of sEH in the retinal Müller glial cells of non-diabetic mice resulted in similar vessel abnormalities to those seen in diabetic mice with retinopathy. Thus, increased expression of sEH is a key determinant in the pathogenesis of diabetic retinopathy, and inhibition of sEH can prevent progression of the disease.

Published
2017

17. Tricuspid Regurgitation and TAVR: Outcomes, Risk Factors and Biomarkers

Author

Puehler, Thomas, primary, Pommert, Nina Sophie, additional, Freitag-Wolf, Sandra, additional, Seoudy, Hatim, additional, Ernst, Markus, additional, Haneya, Assad, additional, Sathananthan, Janarthanan, additional, Sellers, Stephanie L., additional, Meier, David, additional, Schöttler, Jan, additional, Müller, Oliver J., additional, Salehi Ravesh, Mona, additional, Saad, Mohammed, additional, Frank, Derk, additional, and Lutter, Georg, additional

Published
2024
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20. Liver alanine catabolism promotes skeletal muscle atrophy and hyperglycaemia in type 2 diabetes

Author

Okun, Jürgen G., Rusu, Patricia M., Chan, Andrea Y., Wu, Yuqin, Yap, Yann W., Sharkie, Thomas, Schumacher, Jonas, Schmidt, Kathrin V., Roberts-Thomson, Katherine M., Russell, Ryan D., Zota, Annika, Hille, Susanne, Jungmann, Andreas, Maggi, Ludovico, Lee, Young, Blüher, Matthias, Herzig, Stephan, Keske, Michelle A., Heikenwalder, Mathias, Müller, Oliver J., and Rose, Adam J.

Published
2021
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21. A roadmap for therapeutic discovery in pulmonary hypertension associated with left heart failure. A scientific statement of the Heart Failure Association (HFA) of the ESC and the ESC Working Group on Pulmonary Circulation & Right Ventricular Function.

Author

Ameri, Pietro, Mercurio, Valentina, Pollesello, Piero, Anker, Markus S., Backs, Johannes, Bayes‐Genis, Antoni, Borlaug, Barry A., Burkhoff, Daniel, Caravita, Sergio, Chan, Stephen Y., de Man, Frances, Giannakoulas, George, González, Aránzazu, Guazzi, Marco, Hassoun, Paul M., Hemnes, Anna R., Maack, Cristoph, Madden, Brendan, Melenovsky, Vojtech, and Müller, Oliver J.

Subjects
PULMONARY circulation, PULMONARY arterial hypertension, HEART failure, PULMONARY hypertension
Abstract

Pulmonary hypertension (PH) associated with left heart failure (LHF) (PH‐LHF) is one of the most common causes of PH. It directly contributes to symptoms and reduced functional capacity and negatively affects right heart function, ultimately leading to a poor prognosis. There are no specific treatments for PH‐LHF, despite the high number of drugs tested so far. This scientific document addresses the main knowledge gaps in PH‐LHF with emphasis on pathophysiology and clinical trials. Key identified issues include better understanding of the role of pulmonary venous versus arteriolar remodelling, multidimensional phenotyping to recognize patient subgroups positioned to respond to different therapies, and conduct of rigorous pre‐clinical studies combining small and large animal models. Advancements in these areas are expected to better inform the design of clinical trials and extend treatment options beyond those effective in pulmonary arterial hypertension. Enrichment strategies, endpoint assessments, and thorough haemodynamic studies, both at rest and during exercise, are proposed to play primary roles to optimize early‐stage development of candidate therapies for PH‐LHF. [ABSTRACT FROM AUTHOR]

Published
2024
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23. AKAP18δ Anchors and Regulates CaMKII Activity at Phospholamban-SERCA2 and RYR

Author

Carlson, Cathrine R., Aronsen, Jan Magnus, Bergan-Dahl, Anna, Moutty, Marie Christine, Lunde, Marianne, Lunde, Per Kristian, Jarstadmarken, Hilde, Wanichawan, Pimthanya, Pereira, Laetitia, Kolstad, Terje RS, Dalhus, Bjørn, Subramanian, Hariharan, Hille, Susanne, Christensen, Geir, Müller, Oliver J., Nikolaev, Viacheslav, Bers, Donald M., Sjaastad, Ivar, Shen, Xin, Louch, William E., Klussmann, Enno, and Sejersted, Ole M.

Published
2021
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24. Producing and Testing Prototype Tissue-Engineered 3D Tri-Leaflet Valved Stents on Biodegradable Poly-ε-Caprolactone Scaffolds

Author

Lutter, Georg, primary, Pommert, Nina Sophie, additional, Zhang, Xiling, additional, Seiler, Jette, additional, Saeid Nia, Monireh, additional, Meier, David, additional, Sellers, Stephanie L., additional, Gorb, Stanislav N., additional, Hansen, Jan-Hinnerk, additional, Seoudy, Hatim, additional, Müller, Oliver J., additional, Saad, Mohammed, additional, Haneya, Assad, additional, Frank, Derk, additional, Puehler, Thomas, additional, and Sathananthan, Janarthanan, additional

Published
2023
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26. Disrupted Binding of Cystathionine γ-Lyase to p53 Promotes Endothelial Senescence

Author

Hu, Jiong, primary, Leisegang, Matthias S., additional, Looso, Mario, additional, Drekolia, Maria-Kyriaki, additional, Wittig, Janina, additional, Mettner, Janina, additional, Karantanou, Christina, additional, Kyselova, Anastasia, additional, Dumbovic, Gabrjela, additional, Li, Xiaoming, additional, Li, Yuanyuan, additional, Guenther, Stefan, additional, John, David, additional, Siragusa, Mauro, additional, Zukunft, Sven, additional, Oo, James A., additional, Wittig, Ilka, additional, Hille, Susanne, additional, Weigert, Andreas, additional, Knapp, Stefan, additional, Brandes, Ralf P., additional, Müller, Oliver J., additional, Papapetropoulos, Andreas, additional, Sigala, Fragiska, additional, Dobreva, Gergana, additional, Kojonazarov, Baktybek, additional, Fleming, Ingrid, additional, and Bibli, Sofia-Iris, additional

Published
2023
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33. The lipid-droplet-associated protein ABHD5 protects the heart through proteolysis of HDAC4

Author

Jebessa, Zegeye H., Shanmukha, Kumar D., Dewenter, Matthias, Lehmann, Lorenz H., Xu, Chang, Schreiter, Friederike, Siede, Dominik, Gong, Xue-Min, Worst, Barbara C., Federico, Giuseppina, Sauer, Sven W., Fischer, Tamas, Wechselberger, Lisa, Müller, Oliver J., Sossalla, Samuel, Dieterich, Christoph, Most, Patrick, Gröne, Herrmann-Josef, Moro, Cedric, Oberer, Monika, Haemmerle, Guenter, Katus, Hugo A., Tyedmers, Jens, and Backs, Johannes

Published
2019
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34. Endovascular interventions in outpatient care

Author

Thieme, Marcus, Krankenberg, Hans, Schilling, Tom, Betge, Stefan, Korosoglou, Grigorios, Rammos, Christos, Vosseler, Markus, Espinola-Klein, Christine, Heilmeier, Britta, Müller, Oliver J., Langhoff, Ralf, Malyar, Nasser, Blessing, Erwin, Caspary, Lutz, Linnemann, Birgit, Heiss, Christian, and Ito, Wulf

Subjects
Medizin, Cardiology and Cardiovascular Medicine
Abstract

Summary: Endovascular arterial revascularisations for the treatment of symptomatic peripheral arterial disease are constantly increasing in importance and number due to the changing age structure and high numbers of comorbidities in the German population. Patients with peripheral artery disease are often at increased risk for peri- and post-procedural complications including severe cardiovascular events. Due to limited financial and human resources and considerable risks of hospitalization, endovascular interventions that were previously reserved for hospitalized patients are now progressively considered to be performed as day case procedures. More than one third of these procedures are performed in Germany by internists with a specialization in angiology. In the current position paper the German Society of Angiology endorsed by the European Society of Vascular Medicine, summarizes the requirements and risk factors to be considered for the planning, safe performance and post procedural care of endovascular revascularizations in outpatients. The performance of endovascular procedures for peripheral artery disease both in hospitalised and outpatients should be accompanied by a mandatory quality assurance process that should not only capture procedural data, but also require documentation of complications and longterm outcome.

Published
2023

35. Incidence of microvascular dysfunction is increased in hyperlipidemic mice, reducing cerebral blood flow and impairing remote memory.

Author

Hernandez Torres, Luis Daniel, Rezende, Flavia, Peschke, Eva, Will, Olga, Hövener, Jan-Bernd, Spiecker, Frauke, Özorhan, Ümit, Lampe, Josephine, Stölting, Ines, Aherrahrou, Zouhair, Künne, Carsten, Kusche-Vihrog, Kristina, Matschl, Urte, Hille, Susanne, Brandes, Ralf P., Schwaninger, Markus, Müller, Oliver J., and Raasch, Walter

Subjects
MICROCIRCULATION disorders, CEREBRAL circulation, MAZE tests, BLOOD flow, CINGULATE cortex, WESTERN diet
Abstract

Introduction: The development of cognitive dysfunction is not necessarily associated with diet-induced obesity. We hypothesized that cognitive dysfunction might require additional vascular damage, for example, in atherosclerotic mice. Methods: We induced atherosclerosis in male C57BL/6N mice by injecting AAV-PCSK9DY (2x1011 VG) and feeding them a cholesterol-rich Western diet. After 3 months, mice were examined for cognition using Barnes maze procedure and for cerebral blood flow. Cerebral vascular morphology was examined by immunehistology. Results: In AAV-PCSK9DY-treated mice, plaque burden, plasma cholesterol, and triglycerides are elevated. RNAseq analyses followed by KEGG annotation show increased expression of genes linked to inflammatory processes in the aortas of these mice. In AAV-PCSK9DY-treated mice learning was delayed and long-term memory impaired. Blood flow was reduced in the cingulate cortex (-17%), caudate putamen (-15%), and hippocampus (-10%). Immunohistological studies also show an increased incidence of string vessels and pericytes (CD31/Col IV staining) in the hippocampus accompanied by patchy blood-brain barrier leaks (IgG staining) and increased macrophage infiltrations (CD68 staining). Discussion: We conclude that the hyperlipidemic PCSK9DY mouse model can serve as an appropriate approach to induce microvascular dysfunction that leads to reduced blood flow in the hippocampus, which could explain the cognitive dysfunction in these mice. [ABSTRACT FROM AUTHOR]

Published
2024
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36. Remodelling of cAMP dynamics within the SERCA2a microdomain in heart failure with preserved ejection fraction caused by obesity and type 2 diabetes.

Author

Lai, Ping, Hille, Susanne S, Subramanian, Hariharan, Wiegmann, Robert, Roser, Pia, Müller, Oliver J, Nikolaev, Viacheslav O, and Jong, Kirstie A De

Subjects
TYPE 2 diabetes, FLUORESCENCE resonance energy transfer, VENTRICULAR ejection fraction, HEART failure, ADENOSINE monophosphate, LEFT ventricular hypertrophy
Abstract

Aims Despite massive efforts, we remain far behind in our attempts to identify effective therapies to treat heart failure with preserved ejection fraction (HFpEF). Diastolic function is critically regulated by sarcoplasmic/endoplasmic reticulum (SR) calcium ATPase 2a (SERCA2a), which forms a functional cardiomyocyte (CM) microdomain where 3′,5′-cyclic adenosine monophosphate (cAMP) produced upon β-adrenergic receptor (β-AR) stimulation leads to phospholamban (PLN) phosphorylation and facilitated Ca2+ re-uptake. Methods and results To visualize real-time cAMP dynamics in the direct vicinity of SERCA2a in healthy and diseased myocytes, we generated a novel mouse model on the leprdb background that stably expresses the Epac1-PLN Förster resonance energy transfer biosensor. Mice homozygous for the leprdb mutation (db/db) developed obesity and type 2 diabetes and presented with a HFpEF phenotype, evident by mild left ventricular hypertrophy and elevated left atria filling pressures. Live cell imaging uncovered a substantial β2-AR subtype stimulated cAMP response within the PLN/SERCA2a microdomain of db/db but not healthy control (db/+) CMs, which was accompanied by increased PLN phosphorylation and accelerated calcium re-uptake. Importantly, db/db CMs also exhibited a desensitization of β1-AR stimulated cAMP pools within the PLN/SERCA2a microdomain, which was accompanied by a blunted lusitropic effect, suggesting that the increased β2-AR control is an intrinsic compensatory mechanism to maintain PLN/SERCA2a-mediated calcium dynamics and cardiac relaxation. Mechanistically, this was due to a local loss of cAMP-degrading phosphodiesterase 4 associated specifically with the PLN/SERCA2a complex. Conclusion These newly identified alterations of cAMP dynamics at the subcellular level in HFpEF should provide mechanistic understanding of microdomain remodelling and pave the way towards new therapies. [ABSTRACT FROM AUTHOR]

Published
2024
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42. Fibin regulates cardiomyocyte hypertrophy and causes protein-aggregate-associated cardiomyopathy in vivo

Author

Petersen, Matthias, primary, Schmiedel, Nesrin, additional, Dierck, Franziska, additional, Hille, Susanne, additional, Remes, Anca, additional, Senger, Frauke, additional, Schmidt, Inga, additional, Lüllmann-Rauch, Renate, additional, Müller, Oliver J., additional, Frank, Derk, additional, Rangrez, Ashraf Y., additional, Frey, Norbert, additional, and Kuhn, Christian, additional

Published
2023
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43. SPSB1‐mediated inhibition of TGF‐β receptor‐II impairs myogenesis in inflammation

Author

Li, Yi, primary, Dörmann, Niklas, additional, Brinschwitz, Björn, additional, Kny, Melanie, additional, Martin, Elisa, additional, Bartels, Kirsten, additional, Li, Ning, additional, Giri, Priyanka Voori, additional, Schwanz, Stefan, additional, Boschmann, Michael, additional, Hille, Susanne, additional, Fielitz, Britta, additional, Wollersheim, Tobias, additional, Grunow, Julius, additional, Felix, Stephan B., additional, Weber‐Carstens, Steffen, additional, Luft, Friedrich C., additional, Müller, Oliver J., additional, and Fielitz, Jens, additional

Published
2023
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45. Dual Functional States of R406W-Desmin Assembly Complexes Cause Cardiomyopathy With Severe Intercalated Disc Derangement in Humans and in Knock-In Mice

Author

Herrmann, Harald, Cabet, Eva, Chevalier, Nicolas R., Moosmann, Julia, Schultheis, Dorothea, Haas, Jan, Schowalter, Mirjam, Berwanger, Carolin, Weyerer, Veronika, Agaimy, Abbas, Meder, Benjamin, Müller, Oliver J., Katus, Hugo A., Schlötzer-Schrehardt, Ursula, Vicart, Patrick, Ferreiro, Ana, Dittrich, Sven, Clemen, Christoph S., Lilienbaum, Alain, and Schröder, Rolf

Published
2020
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46. Restriction of essential amino acids dictates the systemic metabolic response to dietary protein dilution

Author

Yap, Yann W., Rusu, Patricia M., Chan, Andrea Y., Fam, Barbara C., Jungmann, Andreas, Solon-Biet, Samantha M., Barlow, Christopher K., Creek, Darren J., Huang, Cheng, Schittenhelm, Ralf B., Morgan, Bruce, Schmoll, Dieter, Kiens, Bente, Piper, Matthew D. W., Heikenwälder, Mathias, Simpson, Stephen J., Bröer, Stefan, Andrikopoulos, Sofianos, Müller, Oliver J., and Rose, Adam J.

Published
2020
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47. 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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49. 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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