@article{MTMT:34474992,
	title = {YB-1 Is a Novel Target for the Inhibition of α-Adrenergic-Induced Hypertrophy},
	url = {https://m2.mtmt.hu/api/publication/34474992},
	author = {Heger, Jacqueline and Partsch, Stefan and Harjung, Claudia and Varga, Zoltán and Baranyai, Tamás and Weiß, Johannes and Kremer, Lea and Locquet, Fabian and Leszek, Przemyslaw and Ágg, Bence and Benczik, Bettina and Ferdinandy, Péter and Schulz, Rainer and Euler, Gerhild},
	doi = {10.3390/ijms25010401},
	journal-iso = {INT J MOL SCI},
	journal = {INTERNATIONAL JOURNAL OF MOLECULAR SCIENCES},
	volume = {25},
	unique-id = {34474992},
	issn = {1661-6596},
	abstract = {Cardiac hypertrophy resulting from sympathetic nervous system activation triggers the development of heart failure. The transcription factor Y-box binding protein 1 (YB-1) can interact with transcription factors involved in cardiac hypertrophy and may thereby interfere with the hypertrophy growth process. Therefore, the question arises as to whether YB-1 influences cardiomyocyte hypertrophy and might thereby influence the development of heart failure. YB-1 expression is downregulated in human heart biopsies of patients with ischemic cardiomyopathy (n = 8), leading to heart failure. To study the impact of reduced YB-1 in cardiac cells, we performed small interfering RNA (siRNA) experiments in H9C2 cells as well as in adult cardiomyocytes (CMs) of rats. The specificity of YB-1 siRNA was analyzed by a miRNA-like off-target prediction assay identifying potential genes. Testing three high-scoring genes by transfecting cardiac cells with YB-1 siRNA did not result in downregulation of these genes in contrast to YB-1, whose downregulation increased hypertrophic growth. Hypertrophic growth was mediated by PI3K under PE stimulation, as well by downregulation with YB-1 siRNA. On the other hand, overexpression of YB-1 in CMs, caused by infection with an adenovirus encoding YB-1 (AdYB-1), prevented hypertrophic growth under α-adrenergic stimulation with phenylephrine (PE), but not under stimulation with growth differentiation factor 15 (GDF15; n = 10–16). An adenovirus encoding the green fluorescent protein (AdGFP) served as the control. YB-1 overexpression enhanced the mRNA expression of the Gq inhibitor regulator of G-protein signaling 2 (RGS2) under PE stimulation (n = 6), potentially explaining its inhibitory effect on PE-induced hypertrophic growth. This study shows that YB-1 protects cardiomyocytes against PE-induced hypertrophic growth. Like in human end-stage heart failure, YB-1 downregulation may cause the heart to lose its protection against hypertrophic stimuli and progress to heart failure. Therefore, the transcription factor YB-1 is a pivotal signaling molecule, providing perspectives for therapeutic approaches.},
	year = {2024},
	eissn = {1422-0067},
	orcid-numbers = {Varga, Zoltán/0000-0002-2758-0784; Baranyai, Tamás/0000-0002-9378-8938; Ágg, Bence/0000-0002-6492-0426; Benczik, Bettina/0000-0003-0379-2181; Ferdinandy, Péter/0000-0002-6424-6806; Schulz, Rainer/0000-0003-3017-0476; Euler, Gerhild/0000-0001-9094-773X}
}

@article{MTMT:32506486,
	title = {Somatostatin and Its Receptors in Myocardial Ischemia/Reperfusion Injury and Cardioprotection},
	url = {https://m2.mtmt.hu/api/publication/32506486},
	author = {Vörös, Imre and Sághy, Éva and Pohóczky, Krisztina and Makkos, András and Onódi, Zsófia and Brenner, Gábor and Baranyai, Tamás and Ágg, Bence and Váradi, Barnabás and Kemény, Ágnes and Leszek, Przemyslaw and Görbe, Anikó and Varga, Zoltán and Giricz, Zoltán and Schulz, Rainer and Helyes, Zsuzsanna and Ferdinandy, Péter},
	doi = {10.3389/fphar.2021.663655},
	journal-iso = {FRONT PHARMACOL},
	journal = {FRONTIERS IN PHARMACOLOGY},
	volume = {12},
	unique-id = {32506486},
	year = {2021},
	eissn = {1663-9812},
	orcid-numbers = {Vörös, Imre/0000-0001-5922-6109; Sághy, Éva/0000-0002-4031-3461; Pohóczky, Krisztina/0000-0003-0385-5162; Makkos, András/0000-0002-0309-4909; Onódi, Zsófia/0000-0002-3746-8016; Brenner, Gábor/0000-0001-7886-2960; Baranyai, Tamás/0000-0002-9378-8938; Ágg, Bence/0000-0002-6492-0426; Kemény, Ágnes/0000-0002-4523-3938; Görbe, Anikó/0000-0003-4908-1094; Varga, Zoltán/0000-0002-2758-0784; Giricz, Zoltán/0000-0003-2036-8665; Ferdinandy, Péter/0000-0002-6424-6806}
}

@article{MTMT:32068433,
	title = {AIM2-driven inflammasome activation in heart failure},
	url = {https://m2.mtmt.hu/api/publication/32068433},
	author = {Onódi, Zsófia and Ruppert, Mihály and Kucsera, Dániel and Sayour, Alex Ali and Tóth, Viktória and Koncsos, Gábor and Novák, Julianna and Brenner, Gábor and Makkos, András and Baranyai, Tamás and Giricz, Zoltán and Görbe, Anikó and Leszek, Przemyslaw and Gyöngyösi, Mariann and Horváth, Iván and Schulz, Rainer and Merkely, Béla Péter and Ferdinandy, Péter and Radovits, Tamás and Varga, Zoltán},
	doi = {10.1093/cvr/cvab202},
	journal-iso = {CARDIOVASC RES},
	journal = {CARDIOVASCULAR RESEARCH},
	volume = {117},
	unique-id = {32068433},
	issn = {0008-6363},
	year = {2021},
	eissn = {1755-3245},
	pages = {2639-2651},
	orcid-numbers = {Onódi, Zsófia/0000-0002-3746-8016; Kucsera, Dániel/0000-0001-9446-847X; Sayour, Alex Ali/0000-0001-7728-4775; Tóth, Viktória/0000-0002-0426-2425; Koncsos, Gábor/0000-0001-5451-8719; Brenner, Gábor/0000-0001-7886-2960; Makkos, András/0000-0002-0309-4909; Baranyai, Tamás/0000-0002-9378-8938; Giricz, Zoltán/0000-0003-2036-8665; Görbe, Anikó/0000-0003-4908-1094; Merkely, Béla Péter/0000-0001-6514-0723; Ferdinandy, Péter/0000-0002-6424-6806; Varga, Zoltán/0000-0002-2758-0784}
}

@article{MTMT:31992276,
	title = {Post-Myocardial Infarction Heart Failure in Closed-chest Coronary Occlusion/Reperfusion Model in Göttingen Minipigs and Landrace Pigs},
	url = {https://m2.mtmt.hu/api/publication/31992276},
	author = {Brenner, Gábor and Giricz, Zoltán and Garamvölgyi, Rita and Makkos, András and Onódi, Zsófia and Sayour, Viktor Nabil and Gergely, Tamás G and Baranyai, Tamás and Petneházy, Örs and Kőrösi, Dénes and Szabó, P. Gergő and Vágó, Hajnalka and Dohy, Zsófia and Czimbalmos, Csilla and Merkely, Béla Péter and Boldin-Adamsky, Swetlana and Feinstein, Elena and Horváth, Iván and Ferdinandy, Péter},
	doi = {10.3791/61901},
	journal-iso = {JOVE-J VIS EXP},
	journal = {JOVE-JOURNAL OF VISUALIZED EXPERIMENTS},
	volume = {2021},
	unique-id = {31992276},
	issn = {1940-087X},
	year = {2021},
	eissn = {1940-087X},
	orcid-numbers = {Brenner, Gábor/0000-0001-7886-2960; Giricz, Zoltán/0000-0003-2036-8665; Garamvölgyi, Rita/0000-0001-7243-7808; Makkos, András/0000-0002-0309-4909; Onódi, Zsófia/0000-0002-3746-8016; Baranyai, Tamás/0000-0002-9378-8938; Petneházy, Örs/0000-0001-9698-5753; Vágó, Hajnalka/0000-0002-3568-3572; Dohy, Zsófia/0000-0002-0706-5179; Czimbalmos, Csilla/0000-0001-6311-9920; Merkely, Béla Péter/0000-0001-6514-0723; Ferdinandy, Péter/0000-0002-6424-6806}
}

@article{MTMT:31203017,
	title = {Hidden Cardiotoxicity of Rofecoxib Can be Revealed in Experimental Models of Ischemia/Reperfusion},
	url = {https://m2.mtmt.hu/api/publication/31203017},
	author = {Brenner, Gábor and Makkos, András and Nagy, Csilla Terézia and Onódi, Zsófia and Sayour, Viktor Nabil and Gergely, Tamás G and Kiss, Bernadett and Görbe, Anikó and Sághy, Éva and Zádori, Zoltán Sándor and Lázár, Bernadette and Baranyai, Tamás and Varga, Richárd Sándor and Husti, Zoltán and Varró, András and Tóthfalusi, László and Schulz, Rainer and Baczkó, István and Giricz, Zoltán and Ferdinandy, Péter},
	doi = {10.3390/cells9030551},
	journal-iso = {CELLS-BASEL},
	journal = {CELLS},
	volume = {9},
	unique-id = {31203017},
	abstract = {Cardiac adverse effects are among the leading causes of the discontinuation of clinical trials and the withdrawal of drugs from the market. The novel concept of 'hidden cardiotoxicity' is defined as cardiotoxicity of a drug that manifests in the diseased (e.g. ischemic/reperfused), but not in the healthy heart or as a drug-induced deterioration of cardiac stress adaptation (e.g. ischemic conditioning). Here, we aimed to test if the cardiotoxicity of a selective COX-2 inhibitor rofecoxib that was revealed during its clinical use, i.e., increased occurrence of proarrhythmic and thrombotic events, could have been revealed in early phases of drug development by using preclinical models of ischemia/reperfusion (I/R) injury. Rats that were treated with rofecoxib or vehicle for four weeks were subjected to 30 min. coronary artery occlusion and 120 min. reperfusion with or without cardioprotection that is induced by ischemic preconditioning (IPC). Rofecoxib increased overall the arrhythmias including ventricular fibrillation (VF) during I/R. The proarrhythmic effect of rofecoxib during I/R was not observed in the IPC group. Rofecoxib prolonged the action potential duration (APD) in isolated papillary muscles, which was not seen in the simulated IPC group. Interestingly, while showing hidden cardiotoxicity manifested as a proarrhythmic effect during I/R, rofecoxib decreased the infarct size and increased the survival of adult rat cardiac myocytes that were subjected to simulated I/R injury. This is the first demonstration that rofecoxib increased acute mortality due to its proarrhythmic effect via increased APD during I/R. Rofecoxib did not interfere with the cardiprotective effect of IPC; moreover, IPC was able to protect against rofecoxib-induced hidden cardiotoxicity. These results show that cardiac safety testing with simple preclinical models of I/R injury uncovers hidden cardiotoxicity of rofecoxib and might reveal the hidden cardiotoxicity of other drugs.},
	keywords = {REPERFUSION INJURY; Electrophysiology; Arrhythmia; cardiotoxicity; COX-2; Pharmacovigilance; ischemic conditioning; Safety testing; Vioxx; hiddentox},
	year = {2020},
	eissn = {2073-4409},
	orcid-numbers = {Brenner, Gábor/0000-0001-7886-2960; Makkos, András/0000-0002-0309-4909; Nagy, Csilla Terézia/0000-0002-3774-0243; Onódi, Zsófia/0000-0002-3746-8016; Kiss, Bernadett/0000-0001-7631-4418; Görbe, Anikó/0000-0003-4908-1094; Sághy, Éva/0000-0002-4031-3461; Zádori, Zoltán Sándor/0000-0001-7312-618X; Lázár, Bernadette/0000-0001-8123-8720; Baranyai, Tamás/0000-0002-9378-8938; Varró, András/0000-0003-0745-3603; Tóthfalusi, László/0000-0003-3089-1003; Baczkó, István/0000-0002-9588-0797; Giricz, Zoltán/0000-0003-2036-8665; Ferdinandy, Péter/0000-0002-6424-6806}
}

@article{MTMT:30789521,
	title = {Glomerular Collagen Deposition and Lipocalin-2 Expression Are Early Signs of Renal Injury in Prediabetic Obese Rats},
	url = {https://m2.mtmt.hu/api/publication/30789521},
	author = {Bukosza, Éva Nóra and Kaucsár, Tamás and Godó, Mária and Lajtár, Enikő and Tod, Pál and Koncsos, Gábor and Varga, Zoltán and Baranyai, Tamás and Nguyen, Minh Tu and Schachner, Helga and Sőti, Csaba and Ferdinandy, Péter and Giricz, Zoltán and Szénási, Gábor and Hamar, Péter},
	doi = {10.3390/ijms20174266},
	journal-iso = {INT J MOL SCI},
	journal = {INTERNATIONAL JOURNAL OF MOLECULAR SCIENCES},
	volume = {20},
	unique-id = {30789521},
	issn = {1661-6596},
	abstract = {Feeding rats with high-fat diet (HFD) with a single streptozotocin (STZ) injection induced obesity, slightly elevated fasting blood glucose and impaired glucose and insulin tolerance, and caused cardiac hypertrophy and mild diastolic dysfunction as published before by Koncsos et al. in 2016. Here we aimed to explore the renal consequences in the same groups of rats. Male Long-Evans rats were fed normal chow (CON; n = 9) or HFD containing 40% lard and were administered STZ at 20 mg/kg (i.p.) at week four (prediabetic rats, PRED, n = 9). At week 21 blood and urine samples were taken and kidney and liver samples were collected for histology, immunohistochemistry and for analysis of gene expression. HFD and STZ increased body weight and visceral adiposity and plasma leptin concentration. Despite hyperleptinemia, plasma C-reactive protein concentration decreased in PRED rats. Immunohistochemistry revealed elevated collagen IV protein expression in the glomeruli, and Lcn2 mRNA expression increased, while Il-1β mRNA expression decreased in both the renal cortex and medulla in PRED vs. CON rats. Kidney histology, urinary protein excretion, plasma creatinine, glomerular Feret diameter, desmin protein expression, and cortical and medullary mRNA expression of TGF-β1, Nrf2, and PPARγ were similar in CON and PRED rats. Reduced AMPKα phosphorylation of the autophagy regulator Akt was the first sign of liver damage, while plasma lipid and liver enzyme concentrations were similar. In conclusion, glomerular collagen deposition and increased lipocalin-2 expression were the early signs of kidney injury, while most biomarkers of inflammation, oxidative stress and fibrosis were negative in the kidneys of obese, prediabetic rats with mild heart and liver injury.},
	keywords = {Inflammation; OBESITY; Collagen Type IV; Lipocalin-2; Renal Injury},
	year = {2019},
	eissn = {1422-0067},
	orcid-numbers = {Kaucsár, Tamás/0000-0003-4460-1265; Tod, Pál/0000-0001-9163-7071; Koncsos, Gábor/0000-0001-5451-8719; Varga, Zoltán/0000-0002-2758-0784; Baranyai, Tamás/0000-0002-9378-8938; Nguyen, Minh Tu/0000-0003-1653-8377; Sőti, Csaba/0000-0002-4057-7678; Ferdinandy, Péter/0000-0002-6424-6806; Giricz, Zoltán/0000-0003-2036-8665; Szénási, Gábor/0000-0002-7350-6091; Hamar, Péter/0000-0002-1095-3564}
}

@article{MTMT:30403335,
	title = {Transcriptional Alterations by Ischaemic Postconditioning in a Pig Infarction Model: Impact on Microvascular Protection},
	url = {https://m2.mtmt.hu/api/publication/30403335},
	author = {Lukovic, Dominika and Gugerell, Alfred and Zlabinger, Katrin and Winkler, Johannes and Pavo, Noemi and Baranyai, Tamás and Giricz, Zoltán and Varga, Zoltán and Riesenhuber, Martin and Spannbauer, Andreas and Traxler, Denise and Jakab, András and Garamvölgyi, Rita and Petneházy, Örs and Pils, Dietmar and Tóth, Levente and Schulz, Rainer and Ferdinandy, Péter and Gyöngyösi, Mariann},
	doi = {10.3390/ijms20020344},
	journal-iso = {INT J MOL SCI},
	journal = {INTERNATIONAL JOURNAL OF MOLECULAR SCIENCES},
	volume = {20},
	unique-id = {30403335},
	issn = {1661-6596},
	keywords = {ACUTE MYOCARDIAL-INFARCTION; Ischemia-reperfusion injury; ischemic postconditioning; Transcriptome; Porcine model},
	year = {2019},
	eissn = {1422-0067},
	orcid-numbers = {Baranyai, Tamás/0000-0002-9378-8938; Giricz, Zoltán/0000-0003-2036-8665; Varga, Zoltán/0000-0002-2758-0784; Garamvölgyi, Rita/0000-0001-7243-7808; Petneházy, Örs/0000-0001-9698-5753; Ferdinandy, Péter/0000-0002-6424-6806}
}

@article{MTMT:32110245,
	title = {Nagarse treatment of cardiac subsarcolemmal and interfibrillar mitochondria accounts for inaccurate quantification of proteins},
	url = {https://m2.mtmt.hu/api/publication/32110245},
	author = {Koncsos, Gábor and Varga, Zoltán and Baranyai, Tamás and Ferdinandy, Péter and Schulz, R. and Giricz, Zoltán and Boengler, K.},
	doi = {10.1016/j.yjmcc.2018.05.029},
	journal-iso = {J MOL CELL CARDIOL},
	journal = {JOURNAL OF MOLECULAR AND CELLULAR CARDIOLOGY},
	volume = {120},
	unique-id = {32110245},
	issn = {0022-2828},
	keywords = {Cardiac & Cardiovascular Systems},
	year = {2018},
	eissn = {1095-8584},
	pages = {5-6},
	orcid-numbers = {Koncsos, Gábor/0000-0001-5451-8719; Varga, Zoltán/0000-0002-2758-0784; Baranyai, Tamás/0000-0002-9378-8938; Ferdinandy, Péter/0000-0002-6424-6806; Giricz, Zoltán/0000-0003-2036-8665}
}

@mastersthesis{MTMT:3419044,
	title = {REMOTE ISCHEMIC CONDITIONING AND ITS MOLECULAR MECHANISM IN THE HEART},
	url = {https://m2.mtmt.hu/api/publication/3419044},
	author = {Baranyai, Tamás},
	doi = {10.14753/SE.2018.2082},
	publisher = {Semmelweis Egyetem},
	unique-id = {3419044},
	year = {2018},
	orcid-numbers = {Baranyai, Tamás/0000-0002-9378-8938}
}

@article{MTMT:3407315,
	title = {Author Correction: MicroRNA interactome analysis predicts post-transcriptional regulation of ADRB2 and PPP3R1 in the hypercholesterolemic myocardium},
	url = {https://m2.mtmt.hu/api/publication/3407315},
	author = {Ágg, Bence and Baranyai, Tamás and Makkos, András and Veto, B and Faragó, Nóra and Zvara, Ágnes and Giricz, Zoltán and Veres, Dániel and Csermely, Péter and Arányi, Tamás and Puskás, László and Varga, Zoltán and Ferdinandy, Péter},
	doi = {10.1038/s41598-018-30163-9},
	journal-iso = {SCI REP},
	journal = {SCIENTIFIC REPORTS},
	volume = {8},
	unique-id = {3407315},
	issn = {2045-2322},
	year = {2018},
	eissn = {2045-2322},
	orcid-numbers = {Ágg, Bence/0000-0002-6492-0426; Baranyai, Tamás/0000-0002-9378-8938; Makkos, András/0000-0002-0309-4909; Giricz, Zoltán/0000-0003-2036-8665; Csermely, Péter/0000-0001-9234-0659; Varga, Zoltán/0000-0002-2758-0784; Ferdinandy, Péter/0000-0002-6424-6806}
}