@CONFERENCE{MTMT:34152354,
	title = {MICRORNA‐MRNA BIOINFORMATICS TARGET PREDICTION IN A RAT MODEL OF VOLUME OVERLOAD‐INDUCED LEFT VENTRICULAR HYPERTROPHY},
	url = {https://m2.mtmt.hu/api/publication/34152354},
	author = {Bencsik, Péter and Gömöri, Kamilla and Pósa, Bence and Kenyeres, Éva and Szabados, Tamara and Ágg, Bence and Váradi, Barnabás and Tóth, Viktória and Ágoston, Gergely and Leprán, István and Hamdani, Nazha and Görbe, Anikó and Ferdinandy, Péter},
	booktitle = {FAMÉ 2023},
	unique-id = {34152354},
	year = {2023},
	pages = {58-58},
	orcid-numbers = {Bencsik, Péter/0000-0003-1936-6232; Kenyeres, Éva/0000-0002-6070-2560; Szabados, Tamara/0000-0001-8920-1666; Görbe, Anikó/0000-0003-4908-1094; Ferdinandy, Péter/0000-0002-6424-6806}
}

@article{MTMT:33834109,
	title = {Új, potenciális gyógyszertámadáspontok azonosítása volumenterhelés-indukálta bal kamrai hipertrófiában mikroRNS-mRNS bioinformatikai célpont predikcióval},
	url = {https://m2.mtmt.hu/api/publication/33834109},
	author = {Bencsik, Péter and Pósa, Bence and Gömöri, Kamilla and Szabados, Tamara and Ágg, Bence Károly and Váradi, Barnabás and Ágoston, Gergely and Leprán, István and Hamdani, Nazha and Ferdinandy, Péter and Görbe, Anikó},
	journal-iso = {CARDIOL HUNG},
	journal = {CARDIOLOGIA HUNGARICA},
	volume = {53},
	unique-id = {33834109},
	issn = {0133-5596},
	year = {2023},
	eissn = {1588-0230},
	pages = {A306-A306},
	orcid-numbers = {Bencsik, Péter/0000-0003-1936-6232; Szabados, Tamara/0000-0001-8920-1666; Ferdinandy, Péter/0000-0002-6424-6806; Görbe, Anikó/0000-0003-4908-1094}
}

@article{MTMT:33619282,
	title = {Cardioprotective efficacy of limb remote ischaemic preconditioning in rats: discrepancy between a meta-analysis and a three-centre in vivo study},
	url = {https://m2.mtmt.hu/api/publication/33619282},
	author = {Sayour, Viktor Nabil and Brenner, Gábor and Makkos, András and Kiss, Bernadett and Kovácsházi, Csenger and Gergely, Tamás G and Aukrust, Sverre Groever and Tian, Huimin and Zenkl, Viktória and Gömöri, Kamilla and Szabados, Tamara and Bencsik, Péter and Heinen, Andre and Schulz, Rainer and Baxter, Gary F and Zuurbier, Coert J and Vokó, Zoltán and Ferdinandy, Péter and Giricz, Zoltán},
	doi = {10.1093/cvr/cvad024},
	journal-iso = {CARDIOVASC RES},
	journal = {CARDIOVASCULAR RESEARCH},
	volume = {119},
	unique-id = {33619282},
	issn = {0008-6363},
	year = {2023},
	eissn = {1755-3245},
	pages = {1336-1351},
	orcid-numbers = {Brenner, Gábor/0000-0001-7886-2960; Makkos, András/0000-0002-0309-4909; Kiss, Bernadett/0000-0001-7631-4418; Kovácsházi, Csenger/0000-0003-0283-9486; Szabados, Tamara/0000-0001-8920-1666; Bencsik, Péter/0000-0003-1936-6232; Schulz, Rainer/0000-0002-4066-4624; Vokó, Zoltán/0000-0002-1004-1848; Ferdinandy, Péter/0000-0002-6424-6806; Giricz, Zoltán/0000-0003-2036-8665}
}

@article{MTMT:33228699,
	title = {Altered Cellular Protein Quality Control System Modulates Cardiomyocyte Function in Volume Overload-Induced Hypertrophy},
	url = {https://m2.mtmt.hu/api/publication/33228699},
	author = {Gömöri, Kamilla and Herwig, Melissa and Hassoun, Roua and Budde, Heidi and Mostafi, Nusratul and Delalat, Simin and Modi, Suvasini and Begovic, Merima and Szabados, Tamara and Pipis, Judit and Morvay, Nikolett and Leprán, István and Kovács, Árpád and Mügge, Andreas and Ferdinandy, Péter and Görbe, Anikó and Bencsik, Péter and Hamdani, Nazha},
	doi = {10.3390/antiox11112210},
	journal-iso = {ANTIOXIDANTS-BASEL},
	journal = {ANTIOXIDANTS},
	volume = {11},
	unique-id = {33228699},
	abstract = {Volume-induced hypertrophy is one of the risk factors for cardiac morbidity and mortality. In addition, mechanical and metabolic dysfunction, aging, and cellular redox balance are also contributing factors to the disease progression. In this study, we used volume overload (VO), which was induced by an aortocaval fistula in 2-month-old male Wistar rats, and sham-operated animals served as control. Functional parameters were measured by transthoracic echocardiography at termination 4- or 8-months after VO. The animals showed hypertrophic remodeling that was accompanied by mechanical dysfunction and increased cardiomyocyte stiffness. These alterations were reversible upon treatment with glutathione. Cardiomyocyte dysfunction was associated with elevated oxidative stress markers with unchanged inflammatory signaling pathways. In addition, we observed altered phosphorylation status of small heat shock proteins 27 and 70 and diminished protease expression caspases 3 compared to the matched control group, indicating an impaired protein quality control system. Such alterations might be attributed to the increased oxidative stress as anticipated from the enhanced titin oxidation, ubiquitination, and the elevation in oxidative stress markers. Our study showed an early pathological response to VO, which manifests in cardiomyocyte mechanical dysfunction and dysregulated signaling pathways associated with enhanced oxidative stress and an impaired protein quality control system.},
	year = {2022},
	eissn = {2076-3921},
	orcid-numbers = {Herwig, Melissa/0000-0003-3245-5504; Szabados, Tamara/0000-0001-8920-1666; Ferdinandy, Péter/0000-0002-6424-6806; Görbe, Anikó/0000-0003-4908-1094; Bencsik, Péter/0000-0003-1936-6232; Hamdani, Nazha/0000-0002-3053-0008}
}

@article{MTMT:32913786,
	title = {Ischemic postconditioning activates cardiac MMP-2 and decreases biglycan level as well as miR-34a-5p and miR-195-5p expression in early reperfusion in a porcine infarction model},
	url = {https://m2.mtmt.hu/api/publication/32913786},
	author = {Szabados, Tamara and Gömöri, Kamilla and Ferdinandy, Péter and Gyongyosi, M. and Görbe, Anikó and Bencsik, Péter},
	doi = {10.1093/cvr/cvac066.074},
	journal-iso = {CARDIOVASC RES},
	journal = {CARDIOVASCULAR RESEARCH},
	volume = {118},
	unique-id = {32913786},
	issn = {0008-6363},
	year = {2022},
	eissn = {1755-3245},
	pages = {i80},
	orcid-numbers = {Szabados, Tamara/0000-0001-8920-1666; Ferdinandy, Péter/0000-0002-6424-6806; Görbe, Anikó/0000-0003-4908-1094; Bencsik, Péter/0000-0003-1936-6232}
}

@article{MTMT:32905141,
	title = {Proprotein Convertase Subtilisin Kexin Type 9 (PCSK9) Deletion but Not Inhibition of Extracellular PCSK9 Reduces Infarct Sizes Ex Vivo but Not In Vivo},
	url = {https://m2.mtmt.hu/api/publication/32905141},
	author = {Schreckenberg, Rolf and Wolf, Annemarie and Szabados, Tamara and Gömöri, Kamilla and Szabó, István Adorján and Ágoston, Gergely and Brenner, Gábor and Bencsik, Péter and Ferdinandy, Péter and Schulz, Rainer and Schlüter, Klaus-Dieter},
	doi = {10.3390/ijms23126512},
	journal-iso = {INT J MOL SCI},
	journal = {INTERNATIONAL JOURNAL OF MOLECULAR SCIENCES},
	volume = {23},
	unique-id = {32905141},
	issn = {1661-6596},
	year = {2022},
	eissn = {1422-0067},
	orcid-numbers = {Szabados, Tamara/0000-0001-8920-1666; Szabó, István Adorján/0000-0002-0351-1581; Ágoston, Gergely/0000-0002-8513-5750; Brenner, Gábor/0000-0001-7886-2960; Bencsik, Péter/0000-0003-1936-6232; Ferdinandy, Péter/0000-0002-6424-6806; Schulz, Rainer/0000-0003-3017-0476; Schlüter, Klaus-Dieter/0000-0002-6093-4919}
}

@article{MTMT:32830295,
	title = {Ca2+/calmodulin-dependent protein kinase II and protein kinase G oxidation contributes to impaired sarcomeric proteins in hypertrophy model},
	url = {https://m2.mtmt.hu/api/publication/32830295},
	author = {Gömöri, Kamilla and Herwig, Melissa and Budde, Heidi and Hassoun, Roua and Mostafi, Nusratul and Zhazykbayeva, Saltanat and Sieme, Marcel and Modi, Suvasini and Szabados, Tamara and Pipis, Judit and Morvay, Nikolett and Leprán, István and Ágoston, Gergely and Baczkó, István and Kovács, Árpád and Mügge, Andreas and Ferdinandy, Péter and Görbe, Anikó and Bencsik, Péter and Hamdani, Nazha},
	doi = {10.1002/ehf2.13973},
	journal-iso = {ESC HEART FAIL},
	journal = {ESC HEART FAILURE},
	volume = {9},
	unique-id = {32830295},
	issn = {2055-5822},
	abstract = {Volume overload (VO) induced hypertrophy is one of the hallmarks to the development of heart diseases. Understanding the compensatory mechanisms involved in this process might help preventing the disease progression.Therefore, the present study used 2 months old Wistar rats, which underwent an aortocaval fistula to develop VO-induced hypertrophy. The animals were subdivided into four different groups, two sham operated animals served as age-matched controls and two groups with aortocaval fistula. Echocardiography was performed prior termination after 4- and 8-month. Functional and molecular changes of several sarcomeric proteins and their signalling pathways involved in the regulation and modulation of cardiomyocyte function were investigated.The model was characterized with preserved ejection fraction in all groups and with elevated heart/body weight ratio, left/right ventricular and atrial weight at 4- and 8-month, which indicates VO-induced hypertrophy. In addition, 8-months groups showed increased left ventricular internal diameter during diastole, RV internal diameter, stroke volume and velocity-time index compared with their age-matched controls. These changes were accompanied by increased Ca2+ sensitivity and titin-based cardiomyocyte stiffness in 8-month VO rats compared with other groups. The altered cardiomyocyte mechanics was associated with phosphorylation deficit of sarcomeric proteins cardiac troponin I, myosin binding protein C and titin, also accompanied with impaired signalling pathways involved in phosphorylation of these sarcomeric proteins in 8-month VO rats compared with age-matched control group. Impaired protein phosphorylation status and dysregulated signalling pathways were associated with significant alterations in the oxidative status of both kinases CaMKII and PKG explaining by this the elevated Ca2+ sensitivity and titin-based cardiomyocyte stiffness and perhaps the development of hypertrophy.Our findings showed VO-induced cardiomyocyte dysfunction via deranged phosphorylation of myofilament proteins and signalling pathways due to increased oxidative state of CaMKII and PKG and this might contribute to the development of hypertrophy.},
	keywords = {HYPERTROPHY; VOLUME-OVERLOAD; Oxidative stress; sarcomeric proteins},
	year = {2022},
	eissn = {2055-5822},
	pages = {2585-2600},
	orcid-numbers = {Szabados, Tamara/0000-0001-8920-1666; Ágoston, Gergely/0000-0002-8513-5750; Baczkó, István/0000-0002-9588-0797; Ferdinandy, Péter/0000-0002-6424-6806; Görbe, Anikó/0000-0003-4908-1094; Bencsik, Péter/0000-0003-1936-6232; Hamdani, Nazha/0000-0002-3053-0008}
}

@mastersthesis{MTMT:32829702,
	title = {CARDIOPROTECTION IN PRECLINICAL ISCHEMIA/ REPERFUSION MODELS},
	url = {https://m2.mtmt.hu/api/publication/32829702},
	author = {Gömöri, Kamilla},
	doi = {10.14753/SE.2021.2528},
	unique-id = {32829702},
	year = {2021}
}

@article{MTMT:32335966,
	title = {Cardioprotection Against Acute Myocardial Infarction by Matrix Metalloproteinase Inhibition in Normo- and Hypercholesterolemia},
	url = {https://m2.mtmt.hu/api/publication/32335966},
	author = {Szabados, Tamara and Gömöri, Kamilla and Dormán, György and Ferdinandy, Péter and Görbe, Anikó and Bencsik, Péter},
	journal-iso = {SCRIPTA MEDICA},
	journal = {SCRIPTA MEDICA},
	volume = {52},
	unique-id = {32335966},
	issn = {1211-3395},
	year = {2021},
	pages = {S41-S41},
	orcid-numbers = {Szabados, Tamara/0000-0001-8920-1666; Dormán, György/0000-0001-7702-2206; Ferdinandy, Péter/0000-0002-6424-6806; Görbe, Anikó/0000-0003-4908-1094; Bencsik, Péter/0000-0003-1936-6232}
}

@article{MTMT:32246214,
	title = {Effect of ischemic postconditioning on activation of matrix metalloproteinases, biglycan level and cardiac miRNa expression in in vivo porcine model of acute myocardial infarction},
	url = {https://m2.mtmt.hu/api/publication/32246214},
	author = {Szabados, Tamara and Gömöri, Kamilla and Pipis, J and Ferdinandy, Péter and Görbe, Anikó and Bencsik, Péter},
	journal-iso = {SCRIPTA MEDICA},
	journal = {SCRIPTA MEDICA},
	volume = {52},
	unique-id = {32246214},
	issn = {1211-3395},
	year = {2021},
	pages = {S32-S32},
	orcid-numbers = {Szabados, Tamara/0000-0001-8920-1666; Ferdinandy, Péter/0000-0002-6424-6806; Görbe, Anikó/0000-0003-4908-1094; Bencsik, Péter/0000-0003-1936-6232}
}