TY - CONF AU - Bencsik, Péter AU - Gömöri, Kamilla AU - Pósa, Bence AU - Kenyeres, Éva AU - Szabados, Tamara AU - Ágg, Bence AU - Váradi, Barnabás AU - Tóth, Viktória AU - Ágoston, Gergely AU - Leprán, István AU - Hamdani, Nazha AU - Görbe, Anikó AU - Ferdinandy, Péter TI - MICRORNA‐MRNA BIOINFORMATICS TARGET PREDICTION IN A RAT MODEL OF VOLUME OVERLOAD‐INDUCED LEFT VENTRICULAR HYPERTROPHY T2 - FAMÉ 2023 PY - 2023 SP - 58 EP - 58 PG - 1 UR - https://m2.mtmt.hu/api/publication/34152354 ID - 34152354 LA - English DB - MTMT ER - TY - JOUR AU - Bencsik, Péter AU - Pósa, Bence AU - Gömöri, Kamilla AU - Szabados, Tamara AU - Ágg, Bence Károly AU - Váradi, Barnabás AU - Ágoston, Gergely AU - Leprán, István AU - Hamdani, Nazha AU - Ferdinandy, Péter AU - Görbe, Anikó TI - Új, potenciális gyógyszertámadáspontok azonosítása volumenterhelés-indukálta bal kamrai hipertrófiában mikroRNS-mRNS bioinformatikai célpont predikcióval JF - CARDIOLOGIA HUNGARICA J2 - CARDIOL HUNG VL - 53 PY - 2023 IS - Suppl. A SP - A306 EP - A306 PG - 1 SN - 0133-5596 UR - https://m2.mtmt.hu/api/publication/33834109 ID - 33834109 LA - English DB - MTMT ER - TY - JOUR AU - Sayour, Viktor Nabil AU - Brenner, Gábor AU - Makkos, András AU - Kiss, Bernadett AU - Kovácsházi, Csenger AU - Gergely, Tamás G AU - Aukrust, Sverre Groever AU - Tian, Huimin AU - Zenkl, Viktória AU - Gömöri, Kamilla AU - Szabados, Tamara AU - Bencsik, Péter AU - Heinen, Andre AU - Schulz, Rainer AU - Baxter, Gary F AU - Zuurbier, Coert J AU - Vokó, Zoltán AU - Ferdinandy, Péter AU - Giricz, Zoltán TI - Cardioprotective efficacy of limb remote ischaemic preconditioning in rats: discrepancy between a meta-analysis and a three-centre in vivo study JF - CARDIOVASCULAR RESEARCH J2 - CARDIOVASC RES VL - 119 PY - 2023 IS - 6 SP - 1336 EP - 1351 PG - 16 SN - 0008-6363 DO - 10.1093/cvr/cvad024 UR - https://m2.mtmt.hu/api/publication/33619282 ID - 33619282 N1 - Export Date: 15 July 2023 CODEN: CVREA LA - English DB - MTMT ER - TY - JOUR AU - Gömöri, Kamilla AU - Herwig, Melissa AU - Hassoun, Roua AU - Budde, Heidi AU - Mostafi, Nusratul AU - Delalat, Simin AU - Modi, Suvasini AU - Begovic, Merima AU - Szabados, Tamara AU - Pipis, Judit AU - Morvay, Nikolett AU - Leprán, István AU - Kovács, Árpád AU - Mügge, Andreas AU - Ferdinandy, Péter AU - Görbe, Anikó AU - Bencsik, Péter AU - Hamdani, Nazha TI - Altered Cellular Protein Quality Control System Modulates Cardiomyocyte Function in Volume Overload-Induced Hypertrophy JF - ANTIOXIDANTS J2 - ANTIOXIDANTS-BASEL VL - 11 PY - 2022 IS - 11 PG - 16 SN - 2076-3921 DO - 10.3390/antiox11112210 UR - https://m2.mtmt.hu/api/publication/33228699 ID - 33228699 AB - 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. LA - English DB - MTMT ER - TY - JOUR AU - Szabados, Tamara AU - Gömöri, Kamilla AU - Ferdinandy, Péter AU - Gyongyosi, M. AU - Görbe, Anikó AU - Bencsik, Péter TI - 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 JF - CARDIOVASCULAR RESEARCH J2 - CARDIOVASC RES VL - 118 PY - 2022 IS - Suppl. 1 SP - i80 PG - 1 SN - 0008-6363 DO - 10.1093/cvr/cvac066.074 UR - https://m2.mtmt.hu/api/publication/32913786 ID - 32913786 LA - English DB - MTMT ER - TY - JOUR AU - Schreckenberg, Rolf AU - Wolf, Annemarie AU - Szabados, Tamara AU - Gömöri, Kamilla AU - Szabó, István Adorján AU - Ágoston, Gergely AU - Brenner, Gábor AU - Bencsik, Péter AU - Ferdinandy, Péter AU - Schulz, Rainer AU - Schlüter, Klaus-Dieter TI - Proprotein Convertase Subtilisin Kexin Type 9 (PCSK9) Deletion but Not Inhibition of Extracellular PCSK9 Reduces Infarct Sizes Ex Vivo but Not In Vivo JF - INTERNATIONAL JOURNAL OF MOLECULAR SCIENCES J2 - INT J MOL SCI VL - 23 PY - 2022 IS - 12 PG - 14 SN - 1661-6596 DO - 10.3390/ijms23126512 UR - https://m2.mtmt.hu/api/publication/32905141 ID - 32905141 N1 - Export Date: 30 August 2022 LA - English DB - MTMT ER - TY - JOUR AU - Gömöri, Kamilla AU - Herwig, Melissa AU - Budde, Heidi AU - Hassoun, Roua AU - Mostafi, Nusratul AU - Zhazykbayeva, Saltanat AU - Sieme, Marcel AU - Modi, Suvasini AU - Szabados, Tamara AU - Pipis, Judit AU - Morvay, Nikolett AU - Leprán, István AU - Ágoston, Gergely AU - Baczkó, István AU - Kovács, Árpád AU - Mügge, Andreas AU - Ferdinandy, Péter AU - Görbe, Anikó AU - Bencsik, Péter AU - Hamdani, Nazha TI - Ca2+/calmodulin-dependent protein kinase II and protein kinase G oxidation contributes to impaired sarcomeric proteins in hypertrophy model JF - ESC HEART FAILURE J2 - ESC HEART FAIL VL - 9 PY - 2022 IS - 4 SP - 2585 EP - 2600 PG - 16 SN - 2055-5822 DO - 10.1002/ehf2.13973 UR - https://m2.mtmt.hu/api/publication/32830295 ID - 32830295 AB - 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. LA - English DB - MTMT ER - TY - THES AU - Gömöri, Kamilla TI - CARDIOPROTECTION IN PRECLINICAL ISCHEMIA/ REPERFUSION MODELS PY - 2021 DO - 10.14753/SE.2021.2528 UR - https://m2.mtmt.hu/api/publication/32829702 ID - 32829702 LA - English DB - MTMT ER - TY - JOUR AU - Szabados, Tamara AU - Gömöri, Kamilla AU - Dormán, György AU - Ferdinandy, Péter AU - Görbe, Anikó AU - Bencsik, Péter TI - Cardioprotection Against Acute Myocardial Infarction by Matrix Metalloproteinase Inhibition in Normo- and Hypercholesterolemia JF - SCRIPTA MEDICA J2 - SCRIPTA MEDICA VL - 52 PY - 2021 IS - Suppl. 1 SP - S41 EP - S41 PG - 1 SN - 1211-3395 UR - https://m2.mtmt.hu/api/publication/32335966 ID - 32335966 LA - English DB - MTMT ER - TY - JOUR AU - Szabados, Tamara AU - Gömöri, Kamilla AU - Pipis, J AU - Ferdinandy, Péter AU - Görbe, Anikó AU - Bencsik, Péter TI - Effect of ischemic postconditioning on activation of matrix metalloproteinases, biglycan level and cardiac miRNa expression in in vivo porcine model of acute myocardial infarction JF - SCRIPTA MEDICA J2 - SCRIPTA MEDICA VL - 52 PY - 2021 IS - Suppl.1 SP - S32 EP - S32 PG - 1 SN - 1211-3395 UR - https://m2.mtmt.hu/api/publication/32246214 ID - 32246214 LA - English DB - MTMT ER -