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1. MondoA drives malignancy in B-ALL through enhanced adaptation to metabolic stress

Author

Sipol, Alexandra, Hameister, Erik, Xue, Busheng, Hofstetter, Julia, Barenboim, Maxim, Öllinger, Rupert, Jain, Gaurav, Prexler, Carolin, Rubio, Rebeca Alba, Baldauf, Michaela C., Franchina, Davide G., Petry, Andreas, Schmäh, Juliane, Thiel, Uwe, Görlach, Agnes, Cario, Gunnar, Brenner, Dirk, Richter, Günther H.S., Grünewald, Thomas G.P., Rad, Roland, Wolf, Elmar, Ruland, Jürgen, Sorensen, Poul H., and Burdach, Stefan E.G.

Published
2022
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10. European contribution to the study of ROS: A summary of the findings and prospects for the future from the COST action BM1203 (EU-ROS)

Author

Egea, Javier, Fabregat, Isabel, Frapart, Yves M., Ghezzi, Pietro, Görlach, Agnes, Kietzmann, Thomas, Kubaichuk, Kateryna, Knaus, Ulla G., Lopez, Manuela G., Olaso-Gonzalez, Gloria, Petry, Andreas, Schulz, Rainer, Vina, Jose, Winyard, Paul, Bernlohr, David, Ruskovska, Tatjana, Touyz, Rhian M., Papapetropoulos, Andreas, Grune, Tilman, Lamas, Santiago, Schmidt, Harald H.H.W., Di Lisa, Fabio, and Daiber, Andreas

Subjects
Basic medicine
Abstract

The European Cooperation in Science and Technology (COST) provides an ideal framework to establish multi-disciplinary research networks. COST Action BM1203 (EU-ROS) represents a consortium of researchers from different disciplines who are dedicated to providing new insights and tools for better understanding redox biology and medicine and, in the long run, to finding new therapeutic strategies to target dysregulated redox processes in various diseases. This report highlights the major achievements of EU-ROS as well as research updates and new perspectives arising from its members. The EU-ROS consortium comprised more than 140 active members who worked together for four years on the topics briefly described below. The formation of reactive oxygen and nitrogen species (RONS) is an established hallmark of our aerobic environment and metabolism but RONS also act as messengers via redox regulation of essential cellular processes. The fact that many diseases have been found to be associated with oxidative stress established the theory of oxidative stress as a trigger of diseases that can be corrected by antioxidant therapy. However, while experimental studies support this thesis, clinical studies still generate controversial results, due to complex pathophysiology of oxidative stress in humans. For future improvement of antioxidant therapy and better understanding of redox-associated disease progression detailed knowledge on the sources and targets of RONS formation and discrimination of their detrimental or beneficial roles is required. In order to advance this important area of biology and medicine, highly synergistic approaches combining a variety of diverse and contrasting disciplines are needed.

Published
2017

11. The epigenetic landscape related to reactive oxygen species formation in the cardiovascular system

Author

Kietzmann, Thomas, Petry, Andreas, Shvetsova, Antonina, Gerhold, Joachim M, and Görlach, Agnes

Subjects
Cardiovascular Diseases, Animals, Humans, Reactive Oxygen Species, Themed Section: Review Articles, Cardiovascular System, Epigenesis, Genetic
Abstract

Cardiovascular diseases are among the leading causes of death worldwide. Reactive oxygen species (ROS) can act as damaging molecules but also represent central hubs in cellular signalling networks. Increasing evidence indicates that ROS play an important role in the pathogenesis of cardiovascular diseases, although the underlying mechanisms and consequences of pathophysiologically elevated ROS in the cardiovascular system are still not completely resolved. More recently, alterations of the epigenetic landscape, which can affect DNA methylation, post-translational histone modifications, ATP-dependent alterations to chromatin and non-coding RNA transcripts, have been considered to be of increasing importance in the pathogenesis of cardiovascular diseases. While it has long been accepted that epigenetic changes are imprinted during development or even inherited and are not changed after reaching the lineage-specific expression profile, it becomes more and more clear that epigenetic modifications are highly dynamic. Thus, they might provide an important link between the actions of ROS and cardiovascular diseases. This review will provide an overview of the role of ROS in modulating the epigenetic landscape in the context of the cardiovascular system.This article is part of a themed section on Redox Biology and Oxidative Stress in Health and Disease. To view the other articles in this section visit http://onlinelibrary.wiley.com/doi/10.1111/bph.v174.12/issuetoc.

Published
2017

12. Immunoproteasome subunit ß5i/LMP7-deficiency in atherosclerosis

Author

Hewing, Bernd, primary, Ludwig, Antje, additional, Dan, Cristian, additional, Pötzsch, Max, additional, Hannemann, Carmen, additional, Petry, Andreas, additional, Lauer, Dilyara, additional, Görlach, Agnes, additional, Kaschina, Elena, additional, Müller, Dominik N., additional, Baumann, Gert, additional, Stangl, Verena, additional, Stangl, Karl, additional, and Wilck, Nicola, additional

Published
2017
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13. European contribution to the study of ROS: A summary of the findings and prospects for the future from the COST action BM1203 (EU-ROS)

Author

Egea, Javier, primary, Fabregat, Isabel, additional, Frapart, Yves M., additional, Ghezzi, Pietro, additional, Görlach, Agnes, additional, Kietzmann, Thomas, additional, Kubaichuk, Kateryna, additional, Knaus, Ulla G., additional, Lopez, Manuela G., additional, Olaso-Gonzalez, Gloria, additional, Petry, Andreas, additional, Schulz, Rainer, additional, Vina, Jose, additional, Winyard, Paul, additional, Abbas, Kahina, additional, Ademowo, Opeyemi S., additional, Afonso, Catarina B., additional, Andreadou, Ioanna, additional, Antelmann, Haike, additional, Antunes, Fernando, additional, Aslan, Mutay, additional, Bachschmid, Markus M., additional, Barbosa, Rui M., additional, Belousov, Vsevolod, additional, Berndt, Carsten, additional, Bernlohr, David, additional, Bertrán, Esther, additional, Bindoli, Alberto, additional, Bottari, Serge P., additional, Brito, Paula M., additional, Carrara, Guia, additional, Casas, Ana I., additional, Chatzi, Afroditi, additional, Chondrogianni, Niki, additional, Conrad, Marcus, additional, Cooke, Marcus S., additional, Costa, João G., additional, Cuadrado, Antonio, additional, My-Chan Dang, Pham, additional, De Smet, Barbara, additional, Debelec–Butuner, Bilge, additional, Dias, Irundika H.K., additional, Dunn, Joe Dan, additional, Edson, Amanda J., additional, El Assar, Mariam, additional, El-Benna, Jamel, additional, Ferdinandy, Péter, additional, Fernandes, Ana S., additional, Fladmark, Kari E., additional, Förstermann, Ulrich, additional, Giniatullin, Rashid, additional, Giricz, Zoltán, additional, Görbe, Anikó, additional, Griffiths, Helen, additional, Hampl, Vaclav, additional, Hanf, Alina, additional, Herget, Jan, additional, Hernansanz-Agustín, Pablo, additional, Hillion, Melanie, additional, Huang, Jingjing, additional, Ilikay, Serap, additional, Jansen-Dürr, Pidder, additional, Jaquet, Vincent, additional, Joles, Jaap A., additional, Kalyanaraman, Balaraman, additional, Kaminskyy, Danylo, additional, Karbaschi, Mahsa, additional, Kleanthous, Marina, additional, Klotz, Lars-Oliver, additional, Korac, Bato, additional, Korkmaz, Kemal Sami, additional, Koziel, Rafal, additional, Kračun, Damir, additional, Krause, Karl-Heinz, additional, Křen, Vladimír, additional, Krieg, Thomas, additional, Laranjinha, João, additional, Lazou, Antigone, additional, Li, Huige, additional, Martínez-Ruiz, Antonio, additional, Matsui, Reiko, additional, McBean, Gethin J., additional, Meredith, Stuart P., additional, Messens, Joris, additional, Miguel, Verónica, additional, Mikhed, Yuliya, additional, Milisav, Irina, additional, Milković, Lidija, additional, Miranda-Vizuete, Antonio, additional, Mojović, Miloš, additional, Monsalve, María, additional, Mouthuy, Pierre-Alexis, additional, Mulvey, John, additional, Münzel, Thomas, additional, Muzykantov, Vladimir, additional, Nguyen, Isabel T.N., additional, Oelze, Matthias, additional, Oliveira, Nuno G., additional, Palmeira, Carlos M., additional, Papaevgeniou, Nikoletta, additional, Pavićević, Aleksandra, additional, Pedre, Brandán, additional, Peyrot, Fabienne, additional, Phylactides, Marios, additional, Pircalabioru, Gratiela G., additional, Pitt, Andrew R., additional, Poulsen, Henrik E., additional, Prieto, Ignacio, additional, Rigobello, Maria Pia, additional, Robledinos-Antón, Natalia, additional, Rodríguez-Mañas, Leocadio, additional, Rolo, Anabela P., additional, Rousset, Francis, additional, Ruskovska, Tatjana, additional, Saraiva, Nuno, additional, Sasson, Shlomo, additional, Schröder, Katrin, additional, Semen, Khrystyna, additional, Seredenina, Tamara, additional, Shakirzyanova, Anastasia, additional, Smith, Geoffrey L., additional, Soldati, Thierry, additional, Sousa, Bebiana C., additional, Spickett, Corinne M., additional, Stancic, Ana, additional, Stasia, Marie José, additional, Steinbrenner, Holger, additional, Stepanić, Višnja, additional, Steven, Sebastian, additional, Tokatlidis, Kostas, additional, Tuncay, Erkan, additional, Turan, Belma, additional, Ursini, Fulvio, additional, Vacek, Jan, additional, Vajnerova, Olga, additional, Valentová, Kateřina, additional, Van Breusegem, Frank, additional, Varisli, Lokman, additional, Veal, Elizabeth A., additional, Yalçın, A. Suha, additional, Yelisyeyeva, Olha, additional, Žarković, Neven, additional, Zatloukalová, Martina, additional, Zielonka, Jacek, additional, Touyz, Rhian M., additional, Papapetropoulos, Andreas, additional, Grune, Tilman, additional, Lamas, Santiago, additional, Schmidt, Harald H.H.W., additional, Di Lisa, Fabio, additional, and Daiber, Andreas, additional

Published
2017
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15. Reactive oxygen species, nutrition, hypoxia and diseases: Problems solved?

Author

Görlach, Agnes, Dimova, Elitsa Y, Petry, Andreas, Martínez-Ruiz, Antonio, Hernansanz-Agustín, Pablo, Rolo, Anabela P, Palmeira, Carlos M, and Kietzmann, Thomas

Subjects
Nucleocytoplasmic Transport Proteins, Diabetes, NF-kappa B, Nutritional Requirements, Diseases, Free radicals, Diets, Pregnancy Proteins, Atherosclerosis, Mitochondria, Oxygen, Oxidative Stress, Metabolism, Diabetes Mellitus, Type 2, Gene Expression Regulation, Neoplasms, Animals, Humans, Obesity, Mitogen-Activated Protein Kinases, Hypoxia, Energy Metabolism, Reactive Oxygen Species, Signal Transduction
Abstract

Within the last twenty years the view on reactive oxygen species (ROS) has changed; they are no longer only considered to be harmful but also necessary for cellular communication and homeostasis in different organisms ranging from bacteria to mammals. In the latter, ROS were shown to modulate diverse physiological processes including the regulation of growth factor signaling, the hypoxic response, inflammation and the immune response. During the last 60-100 years the life style, at least in the Western world, has changed enormously. This became obvious with an increase in caloric intake, decreased energy expenditure as well as the appearance of alcoholism and smoking; These changes were shown to contribute to generation of ROS which are, at least in part, associated with the occurrence of several chronic diseases like adiposity, atherosclerosis, type II diabetes, and cancer. In this review we discuss aspects and problems on the role of intracellular ROS formation and nutrition with the link to diseases and their problematic therapeutical issues.

Published
2015

24. The HIF1 target gene NOX2 promotes angiogenesis through urotensin-II.

Author

Diebold, Isabel, Petry, Andreas, Sabrane, Karim, Djordjevic, Talija, Hess, John, and rlach, Agnes Gö

Subjects
*NEOVASCULARIZATION, *UROTENSINS, *VASOACTIVE intestinal peptide, *VASCULAR endothelial growth factors, *BLOOD vessels
Abstract

Urotensin-II (U-II) has been considered as one of the most potent vasoactive peptides, although its physiological and pathophysiological role is still not finally resolved. Recent evidence suggests that it promotes angiogenic responses in endothelial cells, although the underlying signalling mechanisms are unclear. Reactive oxygen species derived from NADPH oxidases are major signalling molecules in the vasculature. Because NOX2 is functional in endothelial cells, we investigated the role of the NOX2-containing NADPH oxidase in U-II-induced angiogenesis and elucidated a possible contribution of hypoxia-inducible factor-1 (HIF-1), the master regulator of hypoxic angiogenesis, in the response to U-II. We found that U-II increases angiogenesis in vitro and in vivo, and these responses were prevented by antioxidants, NOX2 knockdown and in Nox2-/- mice. In addition, U-II-induced angiogenesis was dependent on HIF-1. Interestingly, U-II increased NOX2 transcription involving HIF-1, and chromatin immunoprecipitation confirmed NOX2 as a target gene of HIF-1. In support, NOX2 levels were greatly diminished in U-II-stimulated isolated vessels derived from mice deficient in endothelial HIF-1. Conversely, reactive oxygen species derived from NOX2 were required for U-II activation of HIF and upregulation of HIF-1. In line with this, U-II-induced upregulation of HIF-1 was absent in Nox2-/- vessels. Collectively, these findings identified HIF-1 and NOX2 as partners acting in concert to promote angiogenesis in response to U-II. Because U-II has been found to be elevated in cardiovascular disorders and in tumour tissues, this feed-forward mechanism could be an interesting anti-angiogenic therapeutic option in these disorders. [ABSTRACT FROM AUTHOR]

Published
2012
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25. European contribution to the study of ROS: A summary of the findings and prospects for the future from the COST action BM1203 (EU-ROS)

Author

YALÇIN, AHMET SUHA, Egea, Javier, Fabregat, Isabel, Frapart, Yves M., Ghezzi, Pietro, Gorlach, Agnes, Kietzmann, Thomas, Kubaichuk, Kateryna, Knaus, Ulla G., Lopez, Manuela G., Olaso-Gonzalez, Gloria, Petry, Andreas, Schulz, Rainer, Vinal, Jose, Winyard, Paul, Abbas, Kahina, Ademowo, Opeyemi S., Afonso, Catarina B., Andreadou, Ioanna, Antelmann, Haike, Antunes, Fernando, Aslan, Mutay, Bachschmid, Markus M., Barbosa, Rui M., Belousov, Vsevolod, Berndt, Carsten, Bernlohr, David, Bertran, Esther, Bindoli, Alberto, Bottari, Serge P., Brito, Paula M., Carrara, Guia, Casas, Ana I., Chatzi, Afroditi, Chondrogianni, Niki, Conrad, Marcus, Cooke, Marcus S., Costa, Joao G., Cuadrado, Antonio, Dang, Pham My-Chan, De Smet, Barbara, Butuner, Bilge Debelec, Dias, Irundika H. K., Dunn, Joe Dan, Edson, Amanda J., El Assar, Mariam, El-Benna, Jamel, Ferdinandy, Peter, Fernandes, Ana S., Fladmark, Kari E., Forstermann, Ulrich, Giniatullin, Rashid, Giricz, Zoltan, Gorbe, Aniko, Griffiths, Helen, Hampl, Vaclav, Hanf, Alina, Herget, Jan, Hernansanz-Agustin, Pablo, Hillion, Melanie, Huang, Jingjing, Ilikay, Serap, Jansen-Durr, Pidder, Jaquet, Vincent, Joles, Jaap A., Kalyanaraman, Balaraman, Kaminskyy, Danylo, Karbaschi, Mahsa, Kleanthous, Marina, Klotz, Lars-Oliver, Korac, Bato, Sami Korkmaz, Kemal, Koziel, Rafal, Kracun, Damir, Krause, Karl-Heinz, Kren, Vladimir, Krieg, Thomas, Laranjinha, Joao, Lazou, Antigone, Li, Huige, Martinez-Ruiz, Antonio, Matsui, Reiko, McBean, Gethin J., Meredith, Stuart P., Messens, Joris, Miguel, Veronica, Mikhed, Yuliya, Milisav, Irina, Milkovic, Lidija, Miranda-Vizuete, Antonio, Mojovic, Milos, Monsalve, Maria, Mouthuy, Pierre-Alexis, Mulvey, John, Munzel, Thomas, Muzykantov, Vladimir, Nguyen, Isabel T. N., Oelze, Matthias, Oliveira, Nuno G., Palmeira, Carlos M., Papaevgeniou, Nikoletta, Pavicevic, Aleksandra, Pedre, Brandan, Peyrot, Fabienne, Phylactides, Marios, Pircalabioru, Gratiela G., Pitt, Andrew R., Poulsen, Henrik E., Prieto, Ignacio, Pia Rigobello, Maria, Robledinos-Anton, Natalia, Rodriguez-Manas, Leocadio, Rolo, Anabela P., Rousset, Francis, Ruskovska, Tatjana, Saraiva, Nuno, Sasson, Shlomo, Schroeder, Katrin, Semen, Khrystyna, Seredenina, Tamara, Shakirzyanova, Anastasia, Smith, Geoffrey L., Soldati, Thierry, Sousa, Bebiana C., Spickett, Corinne M., Stancic, Ana, Stasia, Marie Jose, Steinbrenner, Holger, Stepanic, Visnja, Steven, Sebastian, Tokatlidis, Kostas, Tuncay, Erkan, Turan, Belma, Ursini, Fulvio, Vacek, Jan, Vajnerova, Olga, Valentova, Katerina, Van Breusegem, Frank, Varisli, Lokman, Veal, Elizabeth A., Yalcin, A. Suha, Yelisyeyeva, Olha, Zarkovic, Neven, Zatloukalova, Martina, Zielonka, Jacek, Touyz, Rhian M., Papapetropoulos, Andreas, Grune, Tilman, Lamas, Santiago, Schmidt, Harald H. H. W., Di Lisa, Fabio, and Daiber, Andreas

Subjects
Redox therapeutics, PULMONARY ARTERIAL-HYPERTENSION, Redox signaling, GROWTH-FACTOR-BETA, Reactive nitrogen species, MICROCYSTIN-INDUCED APOPTOSIS, Antioxidants, MANGANESE SUPEROXIDE-DISMUTASE, CHRONIC GRANULOMATOUS-DISEASE, ENDOPLASMIC-RETICULUM STRESS, Oxidative stress, ENDOTHELIAL-CELL MIGRATION, ADENINE-DINUCLEOTIDE PHOSPHATE, NITRIC-OXIDE SYNTHASE, Reactive oxygen species, MITOCHONDRIAL OXIDATIVE STRESS
Abstract

The European Cooperation in Science and Technology (COST) provides an ideal framework to establish multi-disciplinary research networks. COST Action BM1203 (EU-ROS) represents a consortium of researchers from different disciplines who are dedicated to providing new insights and tools for better understanding redox biology and medicine and, in the long run, to finding new therapeutic strategies to target dysregulated redox processes in various diseases. This report highlights the major achievements of EU-ROS as well as research updates and new perspectives arising from its members. The EU-ROS consortium comprised more than 140 active members who worked together for four years on the topics briefly described below. The formation of reactive oxygen and nitrogen species (RONS) is an established hallmark of our aerobic environment and metabolism but RONS also act as messengers via redox regulation of essential cellular processes. The fact that many diseases have been found to be associated with oxidative stress established the theory of oxidative stress as a trigger of diseases that can be corrected by antioxidant therapy. However, while experimental studies support this thesis, clinical studies still generate controversial results, due to complex pathophysiology of oxidative stress in humans. For future improvement of antioxidant therapy and better understanding of redox-associated disease progression detailed knowledge on the sources and targets of RONS formation and discrimination of their detrimental or beneficial roles is required. In order to advance this important area of biology and medicine, highly synergistic approaches combining a variety of diverse and contrasting disciplines are needed.

Published
2017

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