TY  - JOUR
AU  - Vujačić-Mirski, Ksenija
AU  - Bruns, Kai
AU  - Kalinović, Sanela
AU  - Oelze, Matthias
AU  - Kröller-Schön, Swenja
AU  - Steven, Sebastian
AU  - Mojović, Miloš
AU  - Korać, Bato
AU  - Münzel, Thomas
AU  - Daiber, Andreas
PY  - 2020
UR  - https://www.mdpi.com/2076-3921/9/5/388
UR  - http://www.ncbi.nlm.nih.gov/pubmed/32384768
UR  - https://radar.ibiss.bg.ac.rs/handle/123456789/3672
AB  - Reactive oxygen and nitrogen species (RONS) cause oxidative damage, which is associated with endothelial dysfunction and cardiovascular disease, but may also contribute to redox signaling. Therefore, their precise detection is important for the evaluation of disease mechanisms. Here, we compared three different methods for the detection of 3-nitrotyrosine (3-NT), a marker of nitro-oxidative stress, in biological samples. Nitrated proteins were generated by incubation with peroxynitrite or 3-morpholino sydnonimine (Sin-1) and subjected to total hydrolysis using pronase, a mixture of different proteases. The 3-NT was then separated by high performance liquid chromatography (HPLC) and quantified by electrochemical detection (ECD, CoulArray) and compared to classical methods, namely enzyme-linked immunosorbent assay (ELISA) and dot blot analysis using specific 3-NT antibodies. Calibration curves for authentic 3-NT (detection limit 10 nM) and a concentration-response pattern for 3-NT obtained from digested nitrated bovine serum albumin (BSA) were highly linear over a wide 3-NT concentration range. Also, ex vivo nitration of protein from heart, isolated mitochondria, and serum/plasma could be quantified using the HPLC/ECD method and was confirmed by LC-MS/MS. Of note, nitro-oxidative damage of mitochondria results in increased superoxide (O2•-) formation rates (measured by dihydroethidium-based HPLC assay), pointing to a self-amplification mechanism of oxidative stress. Based on our ex vivo data, the CoulArray quantification method for 3-NT seems to have some advantages regarding sensitivity and selectivity. Establishing a reliable automated HPLC assay for the routine quantification of 3-NT in biological samples of cell culture, of animal and human origin seems to be more sophisticated than expected.
T2  - Antioxidants (Basel, Switzerland)
T2  - Antioxidants (Basel, Switzerland)
T1  - Development of an Analytical Assay for Electrochemical Detection and Quantification of Protein-Bound 3-Nitrotyrosine in Biological Samples and Comparison with Classical, Antibody-Based Methods.
IS  - 5
VL  - 9
DO  - 10.3390/antiox9050388
SP  - 388
ER  - 

@article{
author = "Vujačić-Mirski, Ksenija and Bruns, Kai and Kalinović, Sanela and Oelze, Matthias and Kröller-Schön, Swenja and Steven, Sebastian and Mojović, Miloš and Korać, Bato and Münzel, Thomas and Daiber, Andreas",
year = "2020",
abstract = "Reactive oxygen and nitrogen species (RONS) cause oxidative damage, which is associated with endothelial dysfunction and cardiovascular disease, but may also contribute to redox signaling. Therefore, their precise detection is important for the evaluation of disease mechanisms. Here, we compared three different methods for the detection of 3-nitrotyrosine (3-NT), a marker of nitro-oxidative stress, in biological samples. Nitrated proteins were generated by incubation with peroxynitrite or 3-morpholino sydnonimine (Sin-1) and subjected to total hydrolysis using pronase, a mixture of different proteases. The 3-NT was then separated by high performance liquid chromatography (HPLC) and quantified by electrochemical detection (ECD, CoulArray) and compared to classical methods, namely enzyme-linked immunosorbent assay (ELISA) and dot blot analysis using specific 3-NT antibodies. Calibration curves for authentic 3-NT (detection limit 10 nM) and a concentration-response pattern for 3-NT obtained from digested nitrated bovine serum albumin (BSA) were highly linear over a wide 3-NT concentration range. Also, ex vivo nitration of protein from heart, isolated mitochondria, and serum/plasma could be quantified using the HPLC/ECD method and was confirmed by LC-MS/MS. Of note, nitro-oxidative damage of mitochondria results in increased superoxide (O2•-) formation rates (measured by dihydroethidium-based HPLC assay), pointing to a self-amplification mechanism of oxidative stress. Based on our ex vivo data, the CoulArray quantification method for 3-NT seems to have some advantages regarding sensitivity and selectivity. Establishing a reliable automated HPLC assay for the routine quantification of 3-NT in biological samples of cell culture, of animal and human origin seems to be more sophisticated than expected.",
journal = "Antioxidants (Basel, Switzerland), Antioxidants (Basel, Switzerland)",
title = "Development of an Analytical Assay for Electrochemical Detection and Quantification of Protein-Bound 3-Nitrotyrosine in Biological Samples and Comparison with Classical, Antibody-Based Methods.",
number = "5",
volume = "9",
doi = "10.3390/antiox9050388",
pages = "388"
}

Vujačić-Mirski, K., Bruns, K., Kalinović, S., Oelze, M., Kröller-Schön, S., Steven, S., Mojović, M., Korać, B., Münzel, T.,& Daiber, A.. (2020). Development of an Analytical Assay for Electrochemical Detection and Quantification of Protein-Bound 3-Nitrotyrosine in Biological Samples and Comparison with Classical, Antibody-Based Methods.. in Antioxidants (Basel, Switzerland), 9(5), 388.
https://doi.org/10.3390/antiox9050388

Vujačić-Mirski K, Bruns K, Kalinović S, Oelze M, Kröller-Schön S, Steven S, Mojović M, Korać B, Münzel T, Daiber A. Development of an Analytical Assay for Electrochemical Detection and Quantification of Protein-Bound 3-Nitrotyrosine in Biological Samples and Comparison with Classical, Antibody-Based Methods.. in Antioxidants (Basel, Switzerland). 2020;9(5):388.
doi:10.3390/antiox9050388 .

Vujačić-Mirski, Ksenija, Bruns, Kai, Kalinović, Sanela, Oelze, Matthias, Kröller-Schön, Swenja, Steven, Sebastian, Mojović, Miloš, Korać, Bato, Münzel, Thomas, Daiber, Andreas, "Development of an Analytical Assay for Electrochemical Detection and Quantification of Protein-Bound 3-Nitrotyrosine in Biological Samples and Comparison with Classical, Antibody-Based Methods." in Antioxidants (Basel, Switzerland), 9, no. 5 (2020):388,
https://doi.org/10.3390/antiox9050388 . .

TY  - JOUR
AU  - Daiber, Andreas
AU  - Kröller-Schön, Swenja
AU  - Frenis, Katie
AU  - Oelze, Matthias
AU  - Kalinović, Sanela
AU  - Vujačić-Mirski, Ksenija
AU  - Kuntić, Marin
AU  - Bayo Jimenez, Maria Teresa
AU  - Helmstädter, Johanna
AU  - Steven, Sebastian
AU  - Korać, Bato
AU  - Münzel, Thomas
PY  - 2019
UR  - https://onlinelibrary.wiley.com/doi/abs/10.1002/biof.1506
UR  - https://radar.ibiss.bg.ac.rs/handle/123456789/3329
AB  - Environmental noise is a well-recognized health risk and part of the external exposome-the World Health Organization estimates that 1 million healthy life years are lost annually in Western Europe alone due to noise-related complications, including increased incidence of hypertension, heart failure, myocardial infarction, and stroke. Previous data suggest that noise works through two paired pathways in a proposed reaction model for noise exposure. As a nonspecific stressor, chronic low-level noise exposure can cause a disruption of sleep and communication leading to annoyance and subsequent sympathetic and endocrine stress responses leading to increased blood pressure, heart rate, stress hormone levels, and in particular more oxidative stress, being responsible for vascular dysfunction and representing changes of the internal exposome. Chronic stress generates cardiovascular risk factors on its own such as increased blood pressure, blood viscosity, blood glucose, and activation of blood coagulation. To this end, persistent chronic noise exposure increases cardiometabolic diseases, including arterial hypertension, coronary artery disease, arrhythmia, heart failure, diabetes mellitus type 2, and stroke. The present review discusses the mechanisms of the nonauditory noise-induced cardiovascular and metabolic consequences, focusing on mental stress signaling pathways, activation of the hypothalamic-pituitary-adrenocortical axis and sympathetic nervous system, the association of these activations with inflammation, and the subsequent onset of oxidative stress and vascular dysfunction. © 2019 BioFactors, 2019.
T2  - BioFactors (Oxford, England)
T1  - Environmental noise induces the release of stress hormones and inflammatory signaling molecules leading to oxidative stress and vascular dysfunction-Signatures of the internal exposome.
DO  - 10.1002/biof.1506
ER  - 

@article{
author = "Daiber, Andreas and Kröller-Schön, Swenja and Frenis, Katie and Oelze, Matthias and Kalinović, Sanela and Vujačić-Mirski, Ksenija and Kuntić, Marin and Bayo Jimenez, Maria Teresa and Helmstädter, Johanna and Steven, Sebastian and Korać, Bato and Münzel, Thomas",
year = "2019",
abstract = "Environmental noise is a well-recognized health risk and part of the external exposome-the World Health Organization estimates that 1 million healthy life years are lost annually in Western Europe alone due to noise-related complications, including increased incidence of hypertension, heart failure, myocardial infarction, and stroke. Previous data suggest that noise works through two paired pathways in a proposed reaction model for noise exposure. As a nonspecific stressor, chronic low-level noise exposure can cause a disruption of sleep and communication leading to annoyance and subsequent sympathetic and endocrine stress responses leading to increased blood pressure, heart rate, stress hormone levels, and in particular more oxidative stress, being responsible for vascular dysfunction and representing changes of the internal exposome. Chronic stress generates cardiovascular risk factors on its own such as increased blood pressure, blood viscosity, blood glucose, and activation of blood coagulation. To this end, persistent chronic noise exposure increases cardiometabolic diseases, including arterial hypertension, coronary artery disease, arrhythmia, heart failure, diabetes mellitus type 2, and stroke. The present review discusses the mechanisms of the nonauditory noise-induced cardiovascular and metabolic consequences, focusing on mental stress signaling pathways, activation of the hypothalamic-pituitary-adrenocortical axis and sympathetic nervous system, the association of these activations with inflammation, and the subsequent onset of oxidative stress and vascular dysfunction. © 2019 BioFactors, 2019.",
journal = "BioFactors (Oxford, England)",
title = "Environmental noise induces the release of stress hormones and inflammatory signaling molecules leading to oxidative stress and vascular dysfunction-Signatures of the internal exposome.",
doi = "10.1002/biof.1506"
}

Daiber, A., Kröller-Schön, S., Frenis, K., Oelze, M., Kalinović, S., Vujačić-Mirski, K., Kuntić, M., Bayo Jimenez, M. T., Helmstädter, J., Steven, S., Korać, B.,& Münzel, T.. (2019). Environmental noise induces the release of stress hormones and inflammatory signaling molecules leading to oxidative stress and vascular dysfunction-Signatures of the internal exposome.. in BioFactors (Oxford, England).
https://doi.org/10.1002/biof.1506

Daiber A, Kröller-Schön S, Frenis K, Oelze M, Kalinović S, Vujačić-Mirski K, Kuntić M, Bayo Jimenez MT, Helmstädter J, Steven S, Korać B, Münzel T. Environmental noise induces the release of stress hormones and inflammatory signaling molecules leading to oxidative stress and vascular dysfunction-Signatures of the internal exposome.. in BioFactors (Oxford, England). 2019;.
doi:10.1002/biof.1506 .

Daiber, Andreas, Kröller-Schön, Swenja, Frenis, Katie, Oelze, Matthias, Kalinović, Sanela, Vujačić-Mirski, Ksenija, Kuntić, Marin, Bayo Jimenez, Maria Teresa, Helmstädter, Johanna, Steven, Sebastian, Korać, Bato, Münzel, Thomas, "Environmental noise induces the release of stress hormones and inflammatory signaling molecules leading to oxidative stress and vascular dysfunction-Signatures of the internal exposome." in BioFactors (Oxford, England) (2019),
https://doi.org/10.1002/biof.1506 . .

TY  - JOUR
AU  - Janković, Aleksandra
AU  - Korać, Aleksandra
AU  - Buzadžić, Biljana
AU  - Stančić, Ana
AU  - Otašević, Vesna
AU  - Ferdinandy, Peter
AU  - Daiber, Andreas
AU  - Korać, Bato
PY  - 2017
UR  - http://radar.ibiss.bg.ac.rs/handle/123456789/6734
AB  - Insulin sensitivity and metabolic homeostasis depend on the capacity of adipose tissue to take up and utilize excess glucose and fatty acids. The key aspects that determine the fuel‐buffering capacity of adipose tissue depend on the physiological levels of the small redox molecule, nitric oxide (NO). In addition to impairment of NO synthesis, excessive formation of the superoxide anion (О2 •–) in adipose tissue may be an important interfering factor diverting the signalling of NO and other reactive oxygen and nitrogen species in obesity, resulting in metabolic dysfunction of adipose tissue over time. Besides its role in relief from superoxide burst, enhanced NO signalling may be responsible for the therapeutic benefits of different superoxide dismutase mimetics, in obesity and experimental diabetes models. This review summarizes the role of NO in adipose tissue and highlights the effects of NO/О2 •– ratio ‘teetering’ as a promising pharmacological target in the metabolic syndrome.
PB  - John Wiley & Sons, Inc
T2  - British Journal of Pharmacology
T1  - Targeting the NO/superoxide ratio in adipose tissue: relevance to obesity and diabetes management
IS  - 12
VL  - 174
DO  - 10.1111/bph.13498
SP  - 1570
EP  - 1590
ER  - 

@article{
author = "Janković, Aleksandra and Korać, Aleksandra and Buzadžić, Biljana and Stančić, Ana and Otašević, Vesna and Ferdinandy, Peter and Daiber, Andreas and Korać, Bato",
year = "2017",
abstract = "Insulin sensitivity and metabolic homeostasis depend on the capacity of adipose tissue to take up and utilize excess glucose and fatty acids. The key aspects that determine the fuel‐buffering capacity of adipose tissue depend on the physiological levels of the small redox molecule, nitric oxide (NO). In addition to impairment of NO synthesis, excessive formation of the superoxide anion (О2 •–) in adipose tissue may be an important interfering factor diverting the signalling of NO and other reactive oxygen and nitrogen species in obesity, resulting in metabolic dysfunction of adipose tissue over time. Besides its role in relief from superoxide burst, enhanced NO signalling may be responsible for the therapeutic benefits of different superoxide dismutase mimetics, in obesity and experimental diabetes models. This review summarizes the role of NO in adipose tissue and highlights the effects of NO/О2 •– ratio ‘teetering’ as a promising pharmacological target in the metabolic syndrome.",
publisher = "John Wiley & Sons, Inc",
journal = "British Journal of Pharmacology",
title = "Targeting the NO/superoxide ratio in adipose tissue: relevance to obesity and diabetes management",
number = "12",
volume = "174",
doi = "10.1111/bph.13498",
pages = "1570-1590"
}

Janković, A., Korać, A., Buzadžić, B., Stančić, A., Otašević, V., Ferdinandy, P., Daiber, A.,& Korać, B.. (2017). Targeting the NO/superoxide ratio in adipose tissue: relevance to obesity and diabetes management. in British Journal of Pharmacology
John Wiley & Sons, Inc., 174(12), 1570-1590.
https://doi.org/10.1111/bph.13498

Janković A, Korać A, Buzadžić B, Stančić A, Otašević V, Ferdinandy P, Daiber A, Korać B. Targeting the NO/superoxide ratio in adipose tissue: relevance to obesity and diabetes management. in British Journal of Pharmacology. 2017;174(12):1570-1590.
doi:10.1111/bph.13498 .

Janković, Aleksandra, Korać, Aleksandra, Buzadžić, Biljana, Stančić, Ana, Otašević, Vesna, Ferdinandy, Peter, Daiber, Andreas, Korać, Bato, "Targeting the NO/superoxide ratio in adipose tissue: relevance to obesity and diabetes management" in British Journal of Pharmacology, 174, no. 12 (2017):1570-1590,
https://doi.org/10.1111/bph.13498 . .

TY  - JOUR
AU  - Golbidi, Saeid
AU  - Daiber, Andreas
AU  - Korać, Bato
AU  - Li, Huige
AU  - Essop, M. Faadiel
AU  - Laher, Ismail
PY  - 2017
UR  - http://link.springer.com/10.1007/s11892-017-0951-7
UR  - https://radar.ibiss.bg.ac.rs/handle/123456789/2891
AB  - Purpose of Review: Obesity and obesity-related diseases, largely resulting from urbanization and behavioral changes, are now of global importance. Energy restriction, though, is associated with health improvements and increased longevity. We review some important mechanisms related to calorie limitation aimed at controlling of metabolic diseases, particularly diabetes. Recent Findings: Calorie restriction triggers a complex series of intricate events, including activation of cellular stress response elements, improved autophagy, modification of apoptosis, and alteration in hormonal balance. Intermittent fasting is not only more acceptable to patients, but it also prevents some of the adverse effects of chronic calorie restriction, especially malnutrition. Summary: There are many somatic and potentially psychologic benefits of fasting or intermittent calorie restriction. However, some behavioral modifications related to abstinence of binge eating following a fasting period are crucial in maintaining the desired favorable outcomes.
T2  - Current Diabetes Reports
T1  - Health Benefits of Fasting and Caloric Restriction
IS  - 12
VL  - 17
DO  - 10.1007/s11892-017-0951-7
SP  - 123
EP  - 123
ER  - 

@article{
author = "Golbidi, Saeid and Daiber, Andreas and Korać, Bato and Li, Huige and Essop, M. Faadiel and Laher, Ismail",
year = "2017",
abstract = "Purpose of Review: Obesity and obesity-related diseases, largely resulting from urbanization and behavioral changes, are now of global importance. Energy restriction, though, is associated with health improvements and increased longevity. We review some important mechanisms related to calorie limitation aimed at controlling of metabolic diseases, particularly diabetes. Recent Findings: Calorie restriction triggers a complex series of intricate events, including activation of cellular stress response elements, improved autophagy, modification of apoptosis, and alteration in hormonal balance. Intermittent fasting is not only more acceptable to patients, but it also prevents some of the adverse effects of chronic calorie restriction, especially malnutrition. Summary: There are many somatic and potentially psychologic benefits of fasting or intermittent calorie restriction. However, some behavioral modifications related to abstinence of binge eating following a fasting period are crucial in maintaining the desired favorable outcomes.",
journal = "Current Diabetes Reports",
title = "Health Benefits of Fasting and Caloric Restriction",
number = "12",
volume = "17",
doi = "10.1007/s11892-017-0951-7",
pages = "123-123"
}

Golbidi, S., Daiber, A., Korać, B., Li, H., Essop, M. F.,& Laher, I.. (2017). Health Benefits of Fasting and Caloric Restriction. in Current Diabetes Reports, 17(12), 123-123.
https://doi.org/10.1007/s11892-017-0951-7

Golbidi S, Daiber A, Korać B, Li H, Essop MF, Laher I. Health Benefits of Fasting and Caloric Restriction. in Current Diabetes Reports. 2017;17(12):123-123.
doi:10.1007/s11892-017-0951-7 .

Golbidi, Saeid, Daiber, Andreas, Korać, Bato, Li, Huige, Essop, M. Faadiel, Laher, Ismail, "Health Benefits of Fasting and Caloric Restriction" in Current Diabetes Reports, 17, no. 12 (2017):123-123,
https://doi.org/10.1007/s11892-017-0951-7 . .

TY  - JOUR
AU  - Egea, Javier
AU  - Fabregat, Isabel
AU  - Frapart, Yves M.
AU  - Ghezzi, Pietro
AU  - Görlach, Agnes
AU  - Kietzmann, Thomas
AU  - Kubaichuk, Kateryna
AU  - Knaus, Ulla G.
AU  - Lopez, Manuela G.
AU  - Olaso-Gonzalez, Gloria
AU  - Petry, Andreas
AU  - Schulz, Rainer
AU  - Vina, Jose
AU  - Winyard, Paul
AU  - Abbas, Kahina
AU  - Ademowo, Opeyemi S.
AU  - Afonso, Catarina B.
AU  - Andreadou, Ioanna
AU  - Antelmann, Haike
AU  - Antunes, Fernando
AU  - Aslan, Mutay
AU  - Bachschmid, Markus M.
AU  - Barbosa, Rui M.
AU  - Belousov, Vsevolod
AU  - Berndt, Carsten
AU  - Bernlohr, David
AU  - Bertrán, Esther
AU  - Bindoli, Alberto
AU  - Bottari, Serge P.
AU  - Brito, Paula M.
AU  - Carrara, Guia
AU  - Casas, Ana I.
AU  - Chatzi, Afroditi
AU  - Chondrogianni, Niki
AU  - Conrad, Marcus
AU  - Cooke, Marcus S.
AU  - Costa, João G.
AU  - Cuadrado, Antonio
AU  - My-Chan Dang, Pham
AU  - De Smet, Barbara
AU  - Debelec-Butuner, Bilge
AU  - Dias, Irundika H.K.
AU  - Dunn, Joe Dan
AU  - Edson, Amanda J.
AU  - El Assar, Mariam
AU  - El-Benna, Jamel
AU  - Ferdinandy, Péter
AU  - Fernandes, Ana S.
AU  - Fladmark, Kari E.
AU  - Förstermann, Ulrich
AU  - Giniatullin, Rashid
AU  - Giricz, Zoltán
AU  - Görbe, Anikó
AU  - Griffiths, Helen
AU  - Hampl, Vaclav
AU  - Hanf, Alina
AU  - Herget, Jan
AU  - Hernansanz-Agustín, Pablo
AU  - Hillion, Melanie
AU  - Huang, Jingjing
AU  - Ilikay, Serap
AU  - Jansen-Dürr, Pidder
AU  - Jaquet, Vincent
AU  - Joles, Jaap A.
AU  - Kalyanaraman, Balaraman
AU  - Kaminskyy, Danylo
AU  - Karbaschi, Mahsa
AU  - Kleanthous, Marina
AU  - Klotz, Lars-Oliver
AU  - Korać, Bato
AU  - Korkmaz, Kemal Sami
AU  - Koziel, Rafal
AU  - Kračun, Damir
AU  - Krause, Karl-Heinz
AU  - Křen, Vladimír
AU  - Krieg, Thomas
AU  - Laranjinha, João
AU  - Lazou, Antigone
AU  - Li, Huige
AU  - Martínez-Ruiz, Antonio
AU  - Matsui, Reiko
AU  - McBean, Gethin J.
AU  - Meredith, Stuart P.
AU  - Messens, Joris
AU  - Miguel, Verónica
AU  - Mikhed, Yuliya
AU  - Milisav, Irina
AU  - Milković, Lidija
AU  - Miranda-Vizuete, Antonio
AU  - Mojović, Miloš
AU  - Monsalve, María
AU  - Mouthuy, Pierre-Alexis
AU  - Mulvey, John
AU  - Münzel, Thomas
AU  - Muzykantov, Vladimir
AU  - Nguyen, Isabel T.N.
AU  - Oelze, Matthias
AU  - Oliveira, Nuno G.
AU  - Palmeira, Carlos M.
AU  - Papaevgeniou, Nikoletta
AU  - Pavićević, Aleksandra
AU  - Pedre, Brandán
AU  - Peyrot, Fabienne
AU  - Phylactides, Marios
AU  - Pircalabioru, Gratiela G.
AU  - Pitt, Andrew R.
AU  - Poulsen, Henrik E.
AU  - Prieto, Ignacio
AU  - Rigobello, Maria Pia
AU  - Robledinos-Antón, Natalia
AU  - Rodríguez-Mañas, Leocadio
AU  - Rolo, Anabela P.
AU  - Rousset, Francis
AU  - Ruskovska, Tatjana
AU  - Saraiva, Nuno
AU  - Sasson, Shlomo
AU  - Schröder, Katrin
AU  - Semen, Khrystyna
AU  - Seredenina, Tamara
AU  - Shakirzyanova, Anastasia
AU  - Smith, Geoffrey L.
AU  - Soldati, Thierry
AU  - Sousa, Bebiana C.
AU  - Spickett, Corinne M.
AU  - Stančić, Ana
AU  - Stasia, Marie José
AU  - Steinbrenner, Holger
AU  - Stepanić, Višnja
AU  - Steven, Sebastian
AU  - Tokatlidis, Kostas
AU  - Tuncay, Erkan
AU  - Turan, Belma
AU  - Ursini, Fulvio
AU  - Vacek, Jan
AU  - Vajnerova, Olga
AU  - Valentová, Kateřina
AU  - Van Breusegem, Frank
AU  - Varisli, Lokman
AU  - Veal, Elizabeth A.
AU  - Yalçın, A. Suha
AU  - Yelisyeyeva, Olha
AU  - Žarković, Neven
AU  - Zatloukalová, Martina
AU  - Zielonka, Jacek
AU  - Touyz, Rhian M.
AU  - Papapetropoulos, Andreas
AU  - Grune, Tilman
AU  - Lamas, Santiago
AU  - Schmidt, Harald H.H.W.
AU  - Di Lisa, Fabio
AU  - Daiber, Andreas
PY  - 2017
UR  - http://linkinghub.elsevier.com/retrieve/pii/S2213231717303373
UR  - https://radar.ibiss.bg.ac.rs/handle/123456789/2778
AB  - 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.
T2  - Redox Biology
T1  - European contribution to the study of ROS: A summary of the findings and prospects for the future from the COST action BM1203 (EU-ROS)
VL  - 13
DO  - 10.1016/j.redox.2017.05.007
SP  - 94
EP  - 162
ER  - 

@article{
author = "Egea, Javier and Fabregat, Isabel and Frapart, Yves M. and Ghezzi, Pietro and Görlach, Agnes and Kietzmann, Thomas and Kubaichuk, Kateryna and Knaus, Ulla G. and Lopez, Manuela G. and Olaso-Gonzalez, Gloria and Petry, Andreas and Schulz, Rainer and Vina, Jose and Winyard, Paul and Abbas, Kahina and Ademowo, Opeyemi S. and Afonso, Catarina B. and Andreadou, Ioanna and Antelmann, Haike and Antunes, Fernando and Aslan, Mutay and Bachschmid, Markus M. and Barbosa, Rui M. and Belousov, Vsevolod and Berndt, Carsten and Bernlohr, David and Bertrán, Esther and Bindoli, Alberto and Bottari, Serge P. and Brito, Paula M. and Carrara, Guia and Casas, Ana I. and Chatzi, Afroditi and Chondrogianni, Niki and Conrad, Marcus and Cooke, Marcus S. and Costa, João G. and Cuadrado, Antonio and My-Chan Dang, Pham and De Smet, Barbara and Debelec-Butuner, Bilge and Dias, Irundika H.K. and Dunn, Joe Dan and Edson, Amanda J. and El Assar, Mariam and El-Benna, Jamel and Ferdinandy, Péter and Fernandes, Ana S. and Fladmark, Kari E. and Förstermann, Ulrich and Giniatullin, Rashid and Giricz, Zoltán and Görbe, Anikó and Griffiths, Helen and Hampl, Vaclav and Hanf, Alina and Herget, Jan and Hernansanz-Agustín, Pablo and Hillion, Melanie and Huang, Jingjing and Ilikay, Serap and Jansen-Dürr, Pidder and Jaquet, Vincent and Joles, Jaap A. and Kalyanaraman, Balaraman and Kaminskyy, Danylo and Karbaschi, Mahsa and Kleanthous, Marina and Klotz, Lars-Oliver and Korać, Bato and Korkmaz, Kemal Sami and Koziel, Rafal and Kračun, Damir and Krause, Karl-Heinz and Křen, Vladimír and Krieg, Thomas and Laranjinha, João and Lazou, Antigone and Li, Huige and Martínez-Ruiz, Antonio and Matsui, Reiko and McBean, Gethin J. and Meredith, Stuart P. and Messens, Joris and Miguel, Verónica and Mikhed, Yuliya and Milisav, Irina and Milković, Lidija and Miranda-Vizuete, Antonio and Mojović, Miloš and Monsalve, María and Mouthuy, Pierre-Alexis and Mulvey, John and Münzel, Thomas and Muzykantov, Vladimir and Nguyen, Isabel T.N. and Oelze, Matthias and Oliveira, Nuno G. and Palmeira, Carlos M. and Papaevgeniou, Nikoletta and Pavićević, Aleksandra and Pedre, Brandán and Peyrot, Fabienne and Phylactides, Marios and Pircalabioru, Gratiela G. and Pitt, Andrew R. and Poulsen, Henrik E. and Prieto, Ignacio and Rigobello, Maria Pia and Robledinos-Antón, Natalia and Rodríguez-Mañas, Leocadio and Rolo, Anabela P. and Rousset, Francis and Ruskovska, Tatjana and Saraiva, Nuno and Sasson, Shlomo and Schröder, Katrin and Semen, Khrystyna and Seredenina, Tamara and Shakirzyanova, Anastasia and Smith, Geoffrey L. and Soldati, Thierry and Sousa, Bebiana C. and Spickett, Corinne M. and Stančić, Ana and Stasia, Marie José and Steinbrenner, Holger and Stepanić, Višnja and Steven, Sebastian and Tokatlidis, Kostas and Tuncay, Erkan and Turan, Belma and Ursini, Fulvio and Vacek, Jan and Vajnerova, Olga and Valentová, Kateřina and Van Breusegem, Frank and Varisli, Lokman and Veal, Elizabeth A. and Yalçın, A. Suha and Yelisyeyeva, Olha and Žarković, Neven and Zatloukalová, Martina and Zielonka, Jacek and Touyz, Rhian M. and Papapetropoulos, Andreas and Grune, Tilman and Lamas, Santiago and Schmidt, Harald H.H.W. and Di Lisa, Fabio and Daiber, Andreas",
year = "2017",
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.",
journal = "Redox Biology",
title = "European contribution to the study of ROS: A summary of the findings and prospects for the future from the COST action BM1203 (EU-ROS)",
volume = "13",
doi = "10.1016/j.redox.2017.05.007",
pages = "94-162"
}

Egea, J., Fabregat, I., Frapart, Y. M., Ghezzi, P., Görlach, A., Kietzmann, T., Kubaichuk, K., Knaus, U. G., Lopez, M. G., Olaso-Gonzalez, G., Petry, A., Schulz, R., Vina, J., Winyard, P., Abbas, K., Ademowo, O. S., Afonso, C. B., Andreadou, I., Antelmann, H., Antunes, F., Aslan, M., Bachschmid, M. M., Barbosa, R. M., Belousov, V., Berndt, C., Bernlohr, D., Bertrán, E., Bindoli, A., Bottari, S. P., Brito, P. M., Carrara, G., Casas, A. I., Chatzi, A., Chondrogianni, N., Conrad, M., Cooke, M. S., Costa, J. G., Cuadrado, A., My-Chan Dang, P., De Smet, B., Debelec-Butuner, B., Dias, I. H.K., Dunn, J. D., Edson, A. J., El Assar, M., El-Benna, J., Ferdinandy, P., Fernandes, A. S., Fladmark, K. E., Förstermann, U., Giniatullin, R., Giricz, Z., Görbe, A., Griffiths, H., Hampl, V., Hanf, A., Herget, J., Hernansanz-Agustín, P., Hillion, M., Huang, J., Ilikay, S., Jansen-Dürr, P., Jaquet, V., Joles, J. A., Kalyanaraman, B., Kaminskyy, D., Karbaschi, M., Kleanthous, M., Klotz, L., Korać, B., Korkmaz, K. S., Koziel, R., Kračun, D., Krause, K., Křen, V., Krieg, T., Laranjinha, J., Lazou, A., Li, H., Martínez-Ruiz, A., Matsui, R., McBean, G. J., Meredith, S. P., Messens, J., Miguel, V., Mikhed, Y., Milisav, I., Milković, L., Miranda-Vizuete, A., Mojović, M., Monsalve, M., Mouthuy, P., Mulvey, J., Münzel, T., Muzykantov, V., Nguyen, I. T.N., Oelze, M., Oliveira, N. G., Palmeira, C. M., Papaevgeniou, N., Pavićević, A., Pedre, B., Peyrot, F., Phylactides, M., Pircalabioru, G. G., Pitt, A. R., Poulsen, H. E., Prieto, I., Rigobello, M. P., Robledinos-Antón, N., Rodríguez-Mañas, L., Rolo, A. P., Rousset, F., Ruskovska, T., Saraiva, N., Sasson, S., Schröder, K., Semen, K., Seredenina, T., Shakirzyanova, A., Smith, G. L., Soldati, T., Sousa, B. C., Spickett, C. M., Stančić, A., Stasia, M. J., Steinbrenner, H., Stepanić, V., Steven, S., Tokatlidis, K., Tuncay, E., Turan, B., Ursini, F., Vacek, J., Vajnerova, O., Valentová, K., Van Breusegem, F., Varisli, L., Veal, E. A., Yalçın, A. S., Yelisyeyeva, O., Žarković, N., Zatloukalová, M., Zielonka, J., Touyz, R. M., Papapetropoulos, A., Grune, T., Lamas, S., Schmidt, H. H.H.W., Di Lisa, F.,& Daiber, A.. (2017). European contribution to the study of ROS: A summary of the findings and prospects for the future from the COST action BM1203 (EU-ROS). in Redox Biology, 13, 94-162.
https://doi.org/10.1016/j.redox.2017.05.007

Egea J, Fabregat I, Frapart YM, Ghezzi P, Görlach A, Kietzmann T, Kubaichuk K, Knaus UG, Lopez MG, Olaso-Gonzalez G, Petry A, Schulz R, Vina J, Winyard P, Abbas K, Ademowo OS, Afonso CB, Andreadou I, Antelmann H, Antunes F, Aslan M, Bachschmid MM, Barbosa RM, Belousov V, Berndt C, Bernlohr D, Bertrán E, Bindoli A, Bottari SP, Brito PM, Carrara G, Casas AI, Chatzi A, Chondrogianni N, Conrad M, Cooke MS, Costa JG, Cuadrado A, My-Chan Dang P, De Smet B, Debelec-Butuner B, Dias IH, Dunn JD, Edson AJ, El Assar M, El-Benna J, Ferdinandy P, Fernandes AS, Fladmark KE, Förstermann U, Giniatullin R, Giricz Z, Görbe A, Griffiths H, Hampl V, Hanf A, Herget J, Hernansanz-Agustín P, Hillion M, Huang J, Ilikay S, Jansen-Dürr P, Jaquet V, Joles JA, Kalyanaraman B, Kaminskyy D, Karbaschi M, Kleanthous M, Klotz L, Korać B, Korkmaz KS, Koziel R, Kračun D, Krause K, Křen V, Krieg T, Laranjinha J, Lazou A, Li H, Martínez-Ruiz A, Matsui R, McBean GJ, Meredith SP, Messens J, Miguel V, Mikhed Y, Milisav I, Milković L, Miranda-Vizuete A, Mojović M, Monsalve M, Mouthuy P, Mulvey J, Münzel T, Muzykantov V, Nguyen IT, Oelze M, Oliveira NG, Palmeira CM, Papaevgeniou N, Pavićević A, Pedre B, Peyrot F, Phylactides M, Pircalabioru GG, Pitt AR, Poulsen HE, Prieto I, Rigobello MP, Robledinos-Antón N, Rodríguez-Mañas L, Rolo AP, Rousset F, Ruskovska T, Saraiva N, Sasson S, Schröder K, Semen K, Seredenina T, Shakirzyanova A, Smith GL, Soldati T, Sousa BC, Spickett CM, Stančić A, Stasia MJ, Steinbrenner H, Stepanić V, Steven S, Tokatlidis K, Tuncay E, Turan B, Ursini F, Vacek J, Vajnerova O, Valentová K, Van Breusegem F, Varisli L, Veal EA, Yalçın AS, Yelisyeyeva O, Žarković N, Zatloukalová M, Zielonka J, Touyz RM, Papapetropoulos A, Grune T, Lamas S, Schmidt HH, Di Lisa F, Daiber A. European contribution to the study of ROS: A summary of the findings and prospects for the future from the COST action BM1203 (EU-ROS). in Redox Biology. 2017;13:94-162.
doi:10.1016/j.redox.2017.05.007 .

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, 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, Bertrán, Esther, Bindoli, Alberto, Bottari, Serge P., Brito, Paula M., Carrara, Guia, Casas, Ana I., Chatzi, Afroditi, Chondrogianni, Niki, Conrad, Marcus, Cooke, Marcus S., Costa, João G., Cuadrado, Antonio, My-Chan Dang, Pham, De Smet, Barbara, Debelec-Butuner, Bilge, Dias, Irundika H.K., Dunn, Joe Dan, Edson, Amanda J., El Assar, Mariam, El-Benna, Jamel, Ferdinandy, Péter, Fernandes, Ana S., Fladmark, Kari E., Förstermann, Ulrich, Giniatullin, Rashid, Giricz, Zoltán, Görbe, Anikó, Griffiths, Helen, Hampl, Vaclav, Hanf, Alina, Herget, Jan, Hernansanz-Agustín, Pablo, Hillion, Melanie, Huang, Jingjing, Ilikay, Serap, Jansen-Dürr, Pidder, Jaquet, Vincent, Joles, Jaap A., Kalyanaraman, Balaraman, Kaminskyy, Danylo, Karbaschi, Mahsa, Kleanthous, Marina, Klotz, Lars-Oliver, Korać, Bato, Korkmaz, Kemal Sami, Koziel, Rafal, Kračun, Damir, Krause, Karl-Heinz, Křen, Vladimír, Krieg, Thomas, Laranjinha, João, Lazou, Antigone, Li, Huige, Martínez-Ruiz, Antonio, Matsui, Reiko, McBean, Gethin J., Meredith, Stuart P., Messens, Joris, Miguel, Verónica, Mikhed, Yuliya, Milisav, Irina, Milković, Lidija, Miranda-Vizuete, Antonio, Mojović, Miloš, Monsalve, María, Mouthuy, Pierre-Alexis, Mulvey, John, Münzel, Thomas, Muzykantov, Vladimir, Nguyen, Isabel T.N., Oelze, Matthias, Oliveira, Nuno G., Palmeira, Carlos M., Papaevgeniou, Nikoletta, Pavićević, Aleksandra, Pedre, Brandán, Peyrot, Fabienne, Phylactides, Marios, Pircalabioru, Gratiela G., Pitt, Andrew R., Poulsen, Henrik E., Prieto, Ignacio, Rigobello, Maria Pia, Robledinos-Antón, Natalia, Rodríguez-Mañas, Leocadio, Rolo, Anabela P., Rousset, Francis, Ruskovska, Tatjana, Saraiva, Nuno, Sasson, Shlomo, Schröder, Katrin, Semen, Khrystyna, Seredenina, Tamara, Shakirzyanova, Anastasia, Smith, Geoffrey L., Soldati, Thierry, Sousa, Bebiana C., Spickett, Corinne M., Stančić, Ana, Stasia, Marie José, Steinbrenner, Holger, Stepanić, Višnja, Steven, Sebastian, Tokatlidis, Kostas, Tuncay, Erkan, Turan, Belma, Ursini, Fulvio, Vacek, Jan, Vajnerova, Olga, Valentová, Kateřina, Van Breusegem, Frank, Varisli, Lokman, Veal, Elizabeth A., Yalçın, A. Suha, Yelisyeyeva, Olha, Žarković, Neven, Zatloukalová, Martina, Zielonka, Jacek, Touyz, Rhian M., Papapetropoulos, Andreas, Grune, Tilman, Lamas, Santiago, Schmidt, Harald H.H.W., Di Lisa, Fabio, Daiber, Andreas, "European contribution to the study of ROS: A summary of the findings and prospects for the future from the COST action BM1203 (EU-ROS)" in Redox Biology, 13 (2017):94-162,
https://doi.org/10.1016/j.redox.2017.05.007 . .

TY  - JOUR
AU  - Janković, Aleksandra
AU  - Korac, Aleksandra
AU  - Buzadžić, Biljana J.
AU  - Otašević, Vesna
AU  - Stančić, Ana
AU  - Daiber, Andreas
AU  - Korać, Bato
PY  - 2015
UR  - https://radar.ibiss.bg.ac.rs/handle/123456789/2326
AB  - Obesity is an energy balance disorder associated with dyslipidemia,
   insulin resistance and diabetes type 2, also summarized with the term
   metabolic syndrome or syndrome X. Increasing evidence points to
   ``adipocyte dysfunction{''}, rather than fat mass accretion per se, as
   the key pathophysiological factor for metabolic complications in
   obesity. The dysfunctional fat tissue in obesity characterizes a failure
   to safely store metabolic substrates into existing hypertrophied
   adipocytes and/or into new preadipocytes recruited for differentiation.
   In this review we briefly summarize the potential of redox imbalance in
   fat tissue as an instigator of adipocyte dysfunction in obesity. We
   reveal the challenge of the adipose redox changes, insights in the
   regulation of healthy expansion of adipose tissue and its reduction,
   leading to glucose and lipids overflow. (C) 2015 Published by Elsevier
   B.V.
T2  - Redox Biology
T1  - Redox implications in adipose tissue (dys)function-A new look at old
 acquaintances
VL  - 6
DO  - 10.1016/j.redox.2015.06.018
SP  - 19
EP  - 32
ER  - 

@article{
author = "Janković, Aleksandra and Korac, Aleksandra and Buzadžić, Biljana J. and Otašević, Vesna and Stančić, Ana and Daiber, Andreas and Korać, Bato",
year = "2015",
abstract = "Obesity is an energy balance disorder associated with dyslipidemia,
   insulin resistance and diabetes type 2, also summarized with the term
   metabolic syndrome or syndrome X. Increasing evidence points to
   ``adipocyte dysfunction{''}, rather than fat mass accretion per se, as
   the key pathophysiological factor for metabolic complications in
   obesity. The dysfunctional fat tissue in obesity characterizes a failure
   to safely store metabolic substrates into existing hypertrophied
   adipocytes and/or into new preadipocytes recruited for differentiation.
   In this review we briefly summarize the potential of redox imbalance in
   fat tissue as an instigator of adipocyte dysfunction in obesity. We
   reveal the challenge of the adipose redox changes, insights in the
   regulation of healthy expansion of adipose tissue and its reduction,
   leading to glucose and lipids overflow. (C) 2015 Published by Elsevier
   B.V.",
journal = "Redox Biology",
title = "Redox implications in adipose tissue (dys)function-A new look at old
 acquaintances",
volume = "6",
doi = "10.1016/j.redox.2015.06.018",
pages = "19-32"
}

Janković, A., Korac, A., Buzadžić, B. J., Otašević, V., Stančić, A., Daiber, A.,& Korać, B.. (2015). Redox implications in adipose tissue (dys)function-A new look at old
 acquaintances. in Redox Biology, 6, 19-32.
https://doi.org/10.1016/j.redox.2015.06.018

Janković A, Korac A, Buzadžić BJ, Otašević V, Stančić A, Daiber A, Korać B. Redox implications in adipose tissue (dys)function-A new look at old
 acquaintances. in Redox Biology. 2015;6:19-32.
doi:10.1016/j.redox.2015.06.018 .

Janković, Aleksandra, Korac, Aleksandra, Buzadžić, Biljana J., Otašević, Vesna, Stančić, Ana, Daiber, Andreas, Korać, Bato, "Redox implications in adipose tissue (dys)function-A new look at old
 acquaintances" in Redox Biology, 6 (2015):19-32,
https://doi.org/10.1016/j.redox.2015.06.018 . .