@article{MTMT:30460033,
	title = {Chronic kidney disease induces left ventricular overexpression of the pro-hypertrophic microRNA-212},
	url = {https://m2.mtmt.hu/api/publication/30460033},
	author = {Sárközy, Márta and Molnár-Gáspár, Renáta and Zvara, Ágnes and Siska, Andrea and Kővári, Bence and Szűcs, Gergő and Márványkövi, Fanni and Kovács, Mónika Gabriella and Diószegi, Petra and Bodai, László and Zsindely, Nóra and Pipicz, Márton and Gömöri, Kamilla and Kiss, Krisztina and Bencsik, Péter and Cserni, Gábor and Puskás, László and Földesi, Imre and Thum, Thomas and Bátkai, Sándor and Csont, Tamás Bálint},
	doi = {10.1038/s41598-018-37690-5},
	journal-iso = {SCI REP},
	journal = {SCIENTIFIC REPORTS},
	volume = {9},
	unique-id = {30460033},
	issn = {2045-2322},
	abstract = {Chronic kidney disease (CKD) is a public health problem that increases the risk of cardiovascular morbidity and mortality. Heart failure with preserved ejection fraction (HFpEF) characterized by left ventricular hypertrophy (LVH) and diastolic dysfunction is a common cardiovascular complication of CKD. MicroRNA-212 (miR-212) has been demonstrated previously to be a crucial regulator of pathologic LVH in pressure-overload-induced heart failure via regulating the forkhead box O3 (FOXO3)/calcineurin/nuclear factor of activated T-cells (NFAT) pathway. Here we aimed to investigate whether miR-212 and its hypertrophy-associated targets including FOXO3, extracellular signal-regulated kinase 2 (ERK2), and AMP-activated protein kinase (AMPK) play a role in the development of HFpEF in CKD. CKD was induced by 5/6 nephrectomy in male Wistar rats. Echocardiography and histology revealed LVH, fibrosis, preserved systolic function, and diastolic dysfunction in the CKD group as compared to sham-operated animals eight and/or nine weeks later. Left ventricular miR-212 was significantly overexpressed in CKD. However, expressions of FOXO3, AMPK, and ERK2 failed to change significantly at the mRNA or protein level. The protein kinase B (AKT)/FOXO3 and AKT/mammalian target of rapamycin (mTOR) pathways are also proposed regulators of LVH induced by pressure-overload. Interestingly, phospho-AKT/total-AKT ratio was increased in CKD without significantly affecting phosphorylation of FOXO3 or mTOR. In summary, cardiac overexpression of miR-212 in CKD failed to affect its previously implicated hypertrophy-associated downstream targets. Thus, the molecular mechanism of the development of LVH in CKD seems to be independent of the FOXO3, ERK1/2, AMPK, and AKT/mTOR-mediated pathways indicating unique features in this form of LVH.},
	year = {2019},
	eissn = {2045-2322},
	orcid-numbers = {Sárközy, Márta/0000-0002-5929-2146; Molnár-Gáspár, Renáta/0000-0001-9673-4532; Kővári, Bence/0000-0002-4498-8781; Szűcs, Gergő/0000-0003-1874-2718; Márványkövi, Fanni/0000-0002-5114-1319; Kovács, Mónika Gabriella/0000-0002-5756-4662; Diószegi, Petra/0000-0001-8109-2266; Bodai, László/0000-0001-8411-626X; Zsindely, Nóra/0000-0002-6189-3100; Pipicz, Márton/0000-0002-0944-1684; Bencsik, Péter/0000-0003-1936-6232; Cserni, Gábor/0000-0003-1344-7744; Földesi, Imre/0000-0002-3329-8136; Csont, Tamás Bálint/0000-0001-5792-2768}
}

@article{MTMT:3348164,
	title = {A myriad of roles of miR-25 in health and disease},
	url = {https://m2.mtmt.hu/api/publication/3348164},
	author = {Sárközy, Márta and Kahán, Zsuzsanna and Csont, Tamás Bálint},
	doi = {10.18632/oncotarget.24662},
	journal-iso = {ONCOTARGET},
	journal = {ONCOTARGET},
	volume = {9},
	unique-id = {3348164},
	year = {2018},
	eissn = {1949-2553},
	pages = {21580-21612},
	orcid-numbers = {Sárközy, Márta/0000-0002-5929-2146; Kahán, Zsuzsanna/0000-0002-5021-8775; Csont, Tamás Bálint/0000-0001-5792-2768}
}

@article{MTMT:3201148,
	title = {Low-Dose Endotoxin Induces Late Preconditioning, Increases Peroxynitrite Formation, and Activates STAT3 in the Rat Heart},
	url = {https://m2.mtmt.hu/api/publication/3201148},
	author = {Pipicz, Márton and Kocsis-Fodor, Gabriella and Sarvary-Arantes, L and Bencsik, Péter and Varga, Zoltán and Ferdinandy, Péter and Csont, Tamás Bálint},
	doi = {10.3390/molecules22030433},
	journal-iso = {MOLECULES},
	journal = {MOLECULES},
	volume = {22},
	unique-id = {3201148},
	issn = {1420-3049},
	abstract = {Administration of low-dose endotoxin (lipopolysaccharide, LPS) 24 h before a lethal ischemia induces pharmacological late preconditioning. The exact mechanism of this phenomenon is not clear. Here we aimed to investigate whether low-dose LPS exerts late effects on peroxynitrite formation and activation of Akt, Erk, and STAT3 in the heart. Male Wistar rats were injected with LPS (S. typhimurium; 0.5 mg/kg i.p.) or saline. Twenty-four hours later, hearts were isolated, perfused for 10 min, and then used for biochemical analyses. LPS pretreatment enhanced cardiac formation of the peroxynitrite marker 3-nitrotyrosine. LPS pretreatment also increased cardiac levels of the peroxynitrite precursor nitric oxide (NO) and superoxide. The activities of Ca2+-independent NO synthase and xanthine oxidoreductase increased in LPS-pretreated hearts. LPS pretreatment resulted in significantly enhanced phosphorylation of STAT3 and non-significantly increased phosphorylation of Akt without affecting the activation of Erk. In separate experiments, isolated working hearts were subjected to 30 min global ischemia and 20 min reperfusion. LPS pretreatment significantly improved ischemia-reperfusion-induced deterioration of cardiac function. We conclude that LPS pretreatment enhances cardiac peroxynitrite formation and activates STAT3 24 h later, which may contribute to LPS-induced late preconditioning.},
	year = {2017},
	eissn = {1420-3049},
	orcid-numbers = {Pipicz, Márton/0000-0002-0944-1684; Kocsis-Fodor, Gabriella/0000-0001-9884-9878; Bencsik, Péter/0000-0003-1936-6232; Varga, Zoltán/0000-0002-2758-0784; Ferdinandy, Péter/0000-0002-6424-6806; Csont, Tamás Bálint/0000-0001-5792-2768}
}

@article{MTMT:3120913,
	title = {The cytoprotective effect of biglycan core protein involves Toll-like receptor 4 signaling in cardiomyocytes},
	url = {https://m2.mtmt.hu/api/publication/3120913},
	author = {Molnár-Gáspár, Renáta and Pipicz, Márton and Hawchar, Fatime and Kovács, Dávid and Djirackor, Luna Kutiti and Görbe, Anikó and Varga, Zoltán and Csontné Kiricsi, Mónika and Petrovski, Goran and Gácser, Attila and Csonka, Csaba and Csont, Tamás Bálint},
	doi = {10.1016/j.yjmcc.2016.08.006},
	journal-iso = {J MOL CELL CARDIOL},
	journal = {JOURNAL OF MOLECULAR AND CELLULAR CARDIOLOGY},
	volume = {99},
	unique-id = {3120913},
	issn = {0022-2828},
	abstract = {Aims Exogenously administered biglycan (core protein with high-molecular weight glycosaminoglycan chains) has been shown to protect neonatal cardiomyocytes against simulated ischemia/reperfusion injury (SI/R), however, the mechanism of action is not clear. In this study we aimed to investigate, which structural component of biglycan is responsible for its cardiocytoprotective effect and to further explore the molecular mechanisms involved in the cytoprotection. Methods and results A pilot study was conducted to demonstrate that both native (glycanated) and deglycanated biglycan can attenuate cell death induced by SI/R in a dose-dependent manner in primary neonatal cardiomyocytes isolated from Wistar rats. In separate experiments, we have shown that similarly to glycanated biglycan, recombinant human biglycan core protein (rhBGNc) protects cardiomyocytes against SI/R injury. In contrast, the glycosaminoglycan component dermatan sulfate had no significant effect on cell viability, while chondroitin sulfate further enhanced cell death induced by SI/R. Treatment of cardiomyocytes with rhBGNc reverses the effect of SI/R upon markers of necrosis, apoptosis, mitochondrial membrane potential, and autophagy. We have also shown that pharmacological blockade of Toll-like receptor 4 (TLR4) signaling or its downstream mediators (IRAK1/4, ERK, JNK and p38 MAP kinases) abolished the cytoprotective effect of rhBGNc against SI/R injury. Pretreatment of cardiomyocytes with rhBGNc for 20 h resulted in increased Akt phosphorylation and NO production without having significant effect on phosphorylation of ERK1/2, STAT3, and on the production of superoxide. Treatment over 10 min and 1 h with rhBGNc increased ERK1 phosphorylation, while the SI/R-induced increase in superoxide production was attenuated by rhBGNc. Blockade of NO synthesis also prevented the cardiocytoprotective effect of rhBGNc. Conclusions The core protein of exogenous biglycan protects myocardial cells from SI/R injury via TLR4-mediated mechanisms involving activation of ERK, JNK and p38 MAP kinases and increased NO production. The cytoprotective effect of rhBGNc is due to modulation of SI/R-induced changes in necrosis, apoptosis and autophagy. © 2016 Elsevier Ltd},
	keywords = {nitric oxide; mitogen activated protein kinase; proteoglycan; protein kinase B; Jun N-terminal kinase},
	year = {2016},
	eissn = {1095-8584},
	pages = {138-150},
	orcid-numbers = {Molnár-Gáspár, Renáta/0000-0001-9673-4532; Pipicz, Márton/0000-0002-0944-1684; Görbe, Anikó/0000-0003-4908-1094; Varga, Zoltán/0000-0002-2758-0784; Csontné Kiricsi, Mónika/0000-0002-8416-2052; Csonka, Csaba/0000-0003-2532-6261; Csont, Tamás Bálint/0000-0001-5792-2768}
}

@article{MTMT:3105323,
	title = {High-dose radiation induced heart damage in a rat model},
	url = {https://m2.mtmt.hu/api/publication/3105323},
	author = {Kiscsatári, Laura and Sárközy, Márta and Kővári, Bence and Varga, Zoltán and Gömöri, Kamilla and Morvay, Nikolett and Leprán, István and Hegyesi, Hargita and Fábián, Gabriella and Cserni, Bálint Gábor and Cserni, Gábor and Csont, Tamás Bálint and Kahán, Zsuzsanna},
	journal-iso = {IN VIVO},
	journal = {IN VIVO},
	volume = {30},
	unique-id = {3105323},
	issn = {0258-851X},
	abstract = {BACKGROUND/AIM: Radiation-induced heart disease (RIHD) is a concern during radiotherapy. For its comprehensive study, an in vivo selective heart irradiation model was developed. MATERIALS AND METHODS: Sprague-Dawley rats were irradiated with 50 Gy and functional imaging, biochemical (circulating growth differentiation factor-15 (GDF-15), transforming growth factor-beta (TGF-beta) and morphological (picrosirius red staining of the heart) objectives were tested. RESULTS: Signs and symptoms of RIHD occurred >12 weeks after irradiation with tachypnea, systolic and diastolic dysfunction, cardiac hypertrophy and body development retardation. Plasma GDF-15 was increased 3, 12 and 26, while plasma TGF-beta was increased 12 weeks after irradiation. At autopsy, extensive pleural fluid was found in the irradiated animals. Interstitial fibrosis could be reliably detected and quantified in irradiated hearts after a follow-up time of 19 weeks. CONCLUSION: The studied parameters could be used in future experiments for testing protective agents for prevention of radiation heart injury.},
	year = {2016},
	eissn = {1791-7549},
	pages = {623-631},
	orcid-numbers = {Sárközy, Márta/0000-0002-5929-2146; Kővári, Bence/0000-0002-4498-8781; Varga, Zoltán/0000-0001-8537-6282; Hegyesi, Hargita/0000-0002-8800-5169; Fábián, Gabriella/0000-0002-2323-4948; Cserni, Gábor/0000-0003-1344-7744; Csont, Tamás Bálint/0000-0001-5792-2768; Kahán, Zsuzsanna/0000-0002-5021-8775}
}

@article{MTMT:3100419,
	title = {Transcriptomic alterations in the heart of non-obese type 2 diabetic Goto-Kakizaki rats},
	url = {https://m2.mtmt.hu/api/publication/3100419},
	author = {Sárközy, Márta and Szűcs, Gergő and Fekete, V and Pipicz, Márton and Eder, K and Molnár-Gáspár, Renáta and Apjok-Sója, Andrea and Pipis, Judit and Ferdinandy, Péter and Csonka, Csaba and Csont, Tamás Bálint},
	doi = {10.1186/s12933-016-0424-3},
	journal-iso = {CARDIOVASC DIABETOL},
	journal = {CARDIOVASCULAR DIABETOLOGY},
	volume = {15},
	unique-id = {3100419},
	issn = {1475-2840},
	abstract = {BACKGROUND: There is a spectacular rise in the global prevalence of type 2 diabetes mellitus (T2DM) due to the worldwide obesity epidemic. However, a significant proportion of T2DM patients are non-obese and they also have an increased risk of cardiovascular diseases. As the Goto-Kakizaki (GK) rat is a well-known model of non-obese T2DM, the goal of this study was to investigate the effect of non-obese T2DM on cardiac alterations of the transcriptome in GK rats. METHODS: Fasting blood glucose, serum insulin and cholesterol levels were measured at 7, 11, and 15 weeks of age in male GK and control rats. Oral glucose tolerance test and pancreatic insulin level measurements were performed at 11 weeks of age. At week 15, total RNA was isolated from the myocardium and assayed by rat oligonucleotide microarray for 41,012 genes, and then expression of selected genes was confirmed by qRT-PCR. Gene ontology and protein-protein network analyses were performed to demonstrate potentially characteristic gene alterations and key genes in non-obese T2DM. RESULTS: Fasting blood glucose, serum insulin and cholesterol levels were significantly increased, glucose tolerance and insulin sensitivity were significantly impaired in GK rats as compared to controls. In hearts of GK rats, 204 genes showed significant up-regulation and 303 genes showed down-regulation as compared to controls according to microarray analysis. Genes with significantly altered expression in the heart due to non-obese T2DM includes functional clusters of metabolism (e.g. Cyp2e1, Akr1b10), signal transduction (e.g. Dpp4, Stat3), receptors and ion channels (e.g. Sln, Chrng), membrane and structural proteins (e.g. Tnni1, Mylk2, Col8a1, Adam33), cell growth and differentiation (e.g. Gpc3, Jund), immune response (e.g. C3, C4a), and others (e.g. Lrp8, Msln, Klkc1, Epn3). Gene ontology analysis revealed several significantly enriched functional inter-relationships between genes influenced by non-obese T2DM. Protein-protein interaction analysis demonstrated that Stat is a potential key gene influenced by non-obese T2DM. CONCLUSIONS: Non-obese T2DM alters cardiac gene expression profile. The altered genes may be involved in the development of cardiac pathologies and could be potential therapeutic targets in non-obese T2DM.},
	year = {2016},
	eissn = {1475-2840},
	orcid-numbers = {Sárközy, Márta/0000-0002-5929-2146; Szűcs, Gergő/0000-0003-1874-2718; Pipicz, Márton/0000-0002-0944-1684; Molnár-Gáspár, Renáta/0000-0001-9673-4532; Apjok-Sója, Andrea/0000-0003-3691-5889; Ferdinandy, Péter/0000-0002-6424-6806; Csonka, Csaba/0000-0003-2532-6261; Csont, Tamás Bálint/0000-0001-5792-2768}
}

@article{MTMT:2966649,
	title = {The soluble guanylate cyclase activator cinaciguat prevents cardiac dysfunction in a rat model of type-1 diabetes mellitus},
	url = {https://m2.mtmt.hu/api/publication/2966649},
	author = {Mátyás, Csaba and Németh, Balázs Tamás and Oláh, Attila and Hidi, László and Birtalan, Ede and Kellermayer, Dalma Lucia and Ruppert, Mihály and Korkmaz-Icoz, S and Kökény, Gábor and Horvath, Eszter Mária and Szabó, Gábor Balázs and Merkely, Béla Péter and Radovits, Tamás},
	doi = {10.1186/s12933-015-0309-x},
	journal-iso = {CARDIOVASC DIABETOL},
	journal = {CARDIOVASCULAR DIABETOLOGY},
	volume = {14},
	unique-id = {2966649},
	issn = {1475-2840},
	abstract = {BACKGROUND: Diabetes mellitus (DM) leads to the development of diabetic cardiomyopathy, which is associated with altered nitric oxide (NO)-soluble guanylate cyclase (sGC)-cyclic guanosine monophosphate (cGMP) signalling. Cardioprotective effects of elevated intracellular cGMP-levels have been described in different heart diseases. In the current study we aimed at investigating the effects of pharmacological activation of sGC in diabetic cardiomyopathy. METHODS: Type-1 DM was induced in rats by streptozotocin. Animals were treated either with the sGC activator cinaciguat (10 mg/kg/day) or with placebo orally for 8 weeks. Left ventricular (LV) pressure-volume (P-V) analysis was used to assess cardiac performance. Additionally, gene expression (qRT-PCR) and protein expression analysis (western blot) were performed. Cardiac structure, markers of fibrotic remodelling and DNA damage were examined by histology, immunohistochemistry and TUNEL assay, respectively. RESULTS: DM was associated with deteriorated cGMP signalling in the myocardium (elevated phosphodiesterase-5 expression, lower cGMP-level and impaired PKG activity). Cardiomyocyte hypertrophy, fibrotic remodelling and DNA fragmentation were present in DM that was associated with impaired LV contractility (preload recruitable stroke work (PRSW): 49.5 +/- 3.3 vs. 83.0 +/- 5.5 mmHg, P < 0.05) and diastolic function (time constant of LV pressure decay (Tau): 17.3 +/- 0.8 vs. 10.3 +/- 0.3 ms, P < 0.05). Cinaciguat treatment effectively prevented DM related molecular, histological alterations and significantly improved systolic (PRSW: 66.8 +/- 3.6 mmHg) and diastolic (Tau: 14.9 +/- 0.6 ms) function. CONCLUSIONS: Cinaciguat prevented structural, molecular alterations and improved cardiac performance of the diabetic heart. Pharmacological activation of sGC might represent a new therapy approach for diabetic cardiomyopathy.},
	year = {2015},
	eissn = {1475-2840},
	orcid-numbers = {Mátyás, Csaba/0000-0001-6095-7611; Németh, Balázs Tamás/0000-0001-7202-8107; Hidi, László/0000-0003-4128-0523; Birtalan, Ede/0000-0002-5699-3545; Kellermayer, Dalma Lucia/0000-0003-0398-0801; Kökény, Gábor/0000-0002-0345-6914; Horvath, Eszter Mária/0000-0002-0517-1269; Merkely, Béla Péter/0000-0001-6514-0723}
}

@article{MTMT:2915576,
	title = {The effect of a preparation of minerals, vitamins and trace elements on the cardiac gene expression pattern in male diabetic rats},
	url = {https://m2.mtmt.hu/api/publication/2915576},
	author = {Sárközy, Márta and Szűcs, Gergő and Pipicz, Márton and Zvara, Ágnes and Eder, K and Fekete, V and Szucs, C and Barkanyi, J and Csonka, Csaba and Puskás, László and Konya, C and Ferdinandy, Péter and Csont, Tamás Bálint},
	doi = {10.1186/s12933-015-0248-6},
	journal-iso = {CARDIOVASC DIABETOL},
	journal = {CARDIOVASCULAR DIABETOLOGY},
	volume = {14},
	unique-id = {2915576},
	issn = {1475-2840},
	abstract = {BACKGROUND: Diabetic patients have an increased risk of developing cardiovascular diseases, which are the leading cause of death in developed countries. Although multivitamin products are widely used as dietary supplements, the effects of these products have not been investigated in the diabetic heart yet. Therefore, here we investigated if a preparation of different minerals, vitamins, and trace elements (MVT) affects the cardiac gene expression pattern in experimental diabetes. METHODS: Two-day old male Wistar rats were injected with streptozotocin (i.p. 100 mg/kg) or citrate buffer to induce diabetes. From weeks 4 to 12, rats were fed with a vehicle or a MVT preparation. Fasting blood glucose measurement and oral glucose tolerance test were performed at week 12, and then total RNA was isolated from the myocardium and assayed by rat oligonucleotide microarray for 41012 oligonucleotides. RESULTS: Significantly elevated fasting blood glucose concentration and impaired glucose tolerance were markedly improved by MVT-treatment in diabetic rats at week 12. Genes with significantly altered expression due to diabetes include functional clusters related to cardiac hypertrophy (e.g. caspase recruitment domain family, member 9; cytochrome P450, family 26, subfamily B, polypeptide; FXYD domain containing ion transport regulator 3), stress response (e.g. metallothionein 1a; metallothionein 2a; interleukin-6 receptor; heme oxygenase (decycling) 1; and glutathione S-transferase, theta 3), and hormones associated with insulin resistance (e.g. resistin; FK506 binding protein 5; galanin/GMAP prepropeptide). Moreover the expression of some other genes with no definite cardiac function was also changed such as e.g. similar to apolipoprotein L2; brain expressed X-linked 1; prostaglandin b2 synthase (brain). MVT-treatment in diabetic rats showed opposite gene expression changes in the cases of 19 genes associated with diabetic cardiomyopathy. In healthy hearts, MVT-treatment resulted in cardiac gene expression changes mostly related to immune response (e.g. complement factor B; complement component 4a; interferon regulatory factor 7; hepcidin). CONCLUSIONS: MVT-treatment improved diagnostic markers of diabetes. This is the first demonstration that MVT-treatment significantly alters cardiac gene expression profile in both control and diabetic rats. Our results and further studies exploring the mechanistic role of individual genes may contribute to the prevention or diagnosis of cardiac complications in diabetes.},
	year = {2015},
	eissn = {1475-2840},
	orcid-numbers = {Sárközy, Márta/0000-0002-5929-2146; Szűcs, Gergő/0000-0003-1874-2718; Pipicz, Márton/0000-0002-0944-1684; Csonka, Csaba/0000-0003-2532-6261; Ferdinandy, Péter/0000-0002-6424-6806; Csont, Tamás Bálint/0000-0001-5792-2768}
}

@article{MTMT:2796784,
	title = {Mechanism and consequences of the shift in cardiac arginine metabolism following ischaemia and reperfusion in rats},
	url = {https://m2.mtmt.hu/api/publication/2796784},
	author = {Schreckenberg, R and Weber, P and Cabrera-Fuentes, HA and Steinert, I and Preissner, KT and Bencsik, Péter and Sárközy, Márta and Csonka, Csaba and Ferdinandy, Péter and Schulz, R and Schluter, KD},
	doi = {10.1160/TH14-05-0477},
	journal-iso = {THROMB HAEMOSTASIS},
	journal = {THROMBOSIS AND HAEMOSTASIS},
	volume = {113},
	unique-id = {2796784},
	issn = {0340-6245},
	abstract = {Cardiac ischaemia and reperfusion leads to irreversible injury and subsequent tissue remodelling. Initial reperfusion seems to shift arginine metabolism from nitric oxide (NO) to polyamine formation. This may limit functional recovery at reperfusion. The hypothesis was tested whether ischaemia/reperfusion translates such a shift in arginine metabolism in a tumour necrosis factor (TNF)-alpha-dependent way and renin-angiotensin system (RAS)-dependent way into a sustained effect. Both, the early post-ischaemic recovery and molecular adaptation to ischaemia/reperfusion were analysed in saline perfused rat hearts undergoing global no-flow ischaemia and reperfusion. Local TNF-alpha activation was blocked by inhibition of TNF-alpha sheddase ADAM17. To interfere with RAS captopril was administered. Arginase was inhibited by administration of Nor-NOHA. Long-term effects of ischemia/reperfusion on arginine metabolism were analysed in vivo in rats receiving an established ischaemia/reperfusion protocol in the closed chest mode. mRNA expression analysis indicated a shift in the arginine metabolism from NO formation to polyamine metabolism starting within 2 hours (h) of reperfusion and translated into protein expression within 24 h. Inhibition of the TNF-alpha pathway and captopril attenuated these delayed effects on post-ischaemic recovery. This shift in arginine metabolism was associated with functional impairment of hearts within 24 h. Inhibition of arginase but not that of TNF-alpha and RAS pathways improved functional recovery immediately. However, no benefit was observed after four months. In conclusion, this study identified TNF-alpha and RAS to be responsible for depressed cardiac function that occurred a few hours after reperfusion.},
	year = {2015},
	eissn = {2567-689X},
	pages = {482-493},
	orcid-numbers = {Bencsik, Péter/0000-0003-1936-6232; Sárközy, Márta/0000-0002-5929-2146; Csonka, Csaba/0000-0003-2532-6261; Ferdinandy, Péter/0000-0002-6424-6806}
}

@article{MTMT:2427091,
	title = {Effect of a multivitamin preparation supplemented with phytosterol on serum lipids and infarct size in rats fed with normal and high cholesterol diet},
	url = {https://m2.mtmt.hu/api/publication/2427091},
	author = {Csont, Tamás Bálint and Sárközy, Márta and Szűcs, Gergő and Szucs, C and Barkanyi, J and Bencsik, Péter and Molnár-Gáspár, Renáta and Földesi, Imre and Csonka, Csaba and Konya, C and Ferdinandy, Péter},
	doi = {10.1186/1476-511X-12-138},
	journal-iso = {LIPIDS HEALTH DIS},
	journal = {LIPIDS IN HEALTH AND DISEASE},
	volume = {12},
	unique-id = {2427091},
	issn = {1476-511X},
	abstract = {BACKGROUND: Although complex multivitamin products are widely used as dietary supplements to maintain health or as special medical food in certain diseases, the effects of these products were not investigated in hyperlipidemia which is a major risk factor for cardiovascular diseases. Therefore, here we investigated if a preparation developed for human use containing different vitamins, minerals and trace elements enriched with phytosterol (VMTP) affects the severity of experimental hyperlipidemia as well as myocardial ischemia/reperfusion injury. METHODS: Male Wistar rats were fed a normal or cholesterol-enriched (2% cholesterol + 0.25% cholate) diet for 12 weeks to induce hyperlipidemia. From week 8, rats in both groups were fed with a VMTP preparation or placebo for 4 weeks. Serum triglyceride and cholesterol levels were measured at week 0, 8 and 12. At week 12, hearts were isolated, perfused according to Langendorff and subjected to a 30-min coronary occlusion followed by 120 min reperfusion to measure infarct size. RESULTS: At week 8, cholesterol-fed rats showed significantly higher serum cholesterol level as compared to normal animals, however, serum triglyceride level did not change. VMTP treatment significantly decreased serum cholesterol level in the hyperlipidemic group by week 12 without affecting triglyceride levels. However, VMTP did not show beneficial effect on infarct size. The inflammatory marker hs-CRP and the antioxidant uric acid were also not significantly different. CONCLUSIONS: This is the first demonstration that treatment of hyperlipidemic subjects with a VMTP preparation reduces serum cholesterol, the major risk factor for cardiovascular disease; however, it does not provide cardioprotection.},
	year = {2013},
	eissn = {1476-511X},
	orcid-numbers = {Csont, Tamás Bálint/0000-0001-5792-2768; Sárközy, Márta/0000-0002-5929-2146; Szűcs, Gergő/0000-0003-1874-2718; Bencsik, Péter/0000-0003-1936-6232; Molnár-Gáspár, Renáta/0000-0001-9673-4532; Földesi, Imre/0000-0002-3329-8136; Csonka, Csaba/0000-0003-2532-6261; Ferdinandy, Péter/0000-0002-6424-6806}
}

@article{MTMT:2176060,
	title = {Metabolic syndrome influences cardiac gene expression pattern at the transcript level in male ZDF rats},
	url = {https://m2.mtmt.hu/api/publication/2176060},
	author = {Sárközy, Márta and Zvara, Ágnes and Gyemant, N and Fekete, V and Kocsis-Fodor, Gabriella and Pipis, Judit and Szűcs, Gergő and Csonka, Csaba and Puskás, László and Ferdinandy, Péter and Csont, Tamás Bálint},
	doi = {10.1186/1475-2840-12-16},
	journal-iso = {CARDIOVASC DIABETOL},
	journal = {CARDIOVASCULAR DIABETOLOGY},
	volume = {12},
	unique-id = {2176060},
	issn = {1475-2840},
	abstract = {ABSTRACT: BACKGROUND: Metabolic syndrome (coexisting visceral obesity, dyslipidemia, hyperglycemia, and hypertension) is a prominent risk factor for cardiovascular morbidity and mortality, however, its effect on cardiac gene expression pattern is unclear. Therefore, we examined the possible alterations in cardiac gene expression pattern in male Zucker Diabetic Fatty (ZDF) rats, a model of metabolic syndrome. METHODS: Fasting blood glucose, serum insulin, cholesterol and triglyceride levels were measured at 6, 16, and 25 wk of age in male ZDF and lean control rats. Oral glucose tolerance test was performed at 16 and 25 wk of age. At week 25, total RNA was isolated from the myocardium and assayed by rat oligonucleotide microarray for 14921 genes. Expression of selected genes was confirmed by qRT-PCR. RESULTS: Fasting blood glucose, serum insulin, cholesterol and triglyceride levels were significantly increased, glucose tolerance and insulin sensitivity were impaired in ZDF rats compared to leans. In hearts of ZDF rats, 36 genes showed significant up-regulation and 49 genes showed down-regulation as compared to lean controls. Genes with significantly altered expression in the heart due to metabolic syndrome includes functional clusters of metabolism (e.g. 3-hydroxy-3-methylglutaryl-Coenzyme A synthase 2; argininosuccinate synthetase; 2-amino-3-ketobutyrate-coenzyme A ligase), structural proteins (e.g. myosin IXA; aggrecan1), signal transduction (e.g. activating transcription factor 3; phospholipase A2; insulin responsive sequence DNA binding protein-1) stress response (e.g. heat shock 70kD protein 1A; heat shock protein 60; glutathione S-transferase Yc2 subunit), ion channels and receptors (e.g. ATPase, (Na+)/K+ transporting, beta 4 polypeptide; ATPase, H+/K+ transporting, nongastric, alpha polypeptide). Moreover some other genes with no definite functional clusters were also changed such as e.g. S100 calcium binding protein A3; ubiquitin carboxy-terminal hydrolase L1; interleukin 18. Gene ontology analysis revealed several significantly enriched functional inter-relationships between genes influenced by metabolic syndrome. CONCLUSIONS: Metabolic syndrome significantly alters cardiac gene expression profile which may be involved in development of cardiac pathologies in the presence of metabolic syndrome.},
	year = {2013},
	eissn = {1475-2840},
	orcid-numbers = {Sárközy, Márta/0000-0002-5929-2146; Kocsis-Fodor, Gabriella/0000-0001-9884-9878; Szűcs, Gergő/0000-0003-1874-2718; Csonka, Csaba/0000-0003-2532-6261; Ferdinandy, Péter/0000-0002-6424-6806; Csont, Tamás Bálint/0000-0001-5792-2768}
}

@article{MTMT:2158757,
	title = {Preconditioning protects the heart in a prolonged uremic condition},
	url = {https://m2.mtmt.hu/api/publication/2158757},
	author = {Kocsis-Fodor, Gabriella and Sárközy, Márta and Bencsik, Péter and Pipicz, Márton and Varga, Zoltán and Pálóczi, János and Csonka, Csaba and Ferdinandy, Péter and Csont, Tamás Bálint},
	doi = {10.1152/ajpheart.00379.2012},
	journal-iso = {AM J PHYSIOL HEART C},
	journal = {AMERICAN JOURNAL OF PHYSIOLOGY: HEART AND CIRCULATORY PHYSIOLOGY},
	volume = {303},
	unique-id = {2158757},
	issn = {0363-6135},
	year = {2012},
	eissn = {1522-1539},
	pages = {H1229-H1236},
	orcid-numbers = {Kocsis-Fodor, Gabriella/0000-0001-9884-9878; Sárközy, Márta/0000-0002-5929-2146; Bencsik, Péter/0000-0003-1936-6232; Pipicz, Márton/0000-0002-0944-1684; Varga, Zoltán/0000-0002-2758-0784; Pálóczi, János/0000-0001-9303-985X; Csonka, Csaba/0000-0003-2532-6261; Ferdinandy, Péter/0000-0002-6424-6806; Csont, Tamás Bálint/0000-0001-5792-2768}
}

@article{MTMT:1406091,
	title = {Dietary red palm oil supplementation reduces myocardial infarct size in an isolated perfused rat heart model},
	url = {https://m2.mtmt.hu/api/publication/1406091},
	author = {Bester, DJ and Kupai, Krisztina and Csont, Tamás Bálint and Szűcs, Gergő and Csonka, Csaba and Esterhuyse, AJ and Ferdinandy, Péter and Van, Rooyen J},
	doi = {10.1186/1476-511X-9-64},
	journal-iso = {LIPIDS HEALTH DIS},
	journal = {LIPIDS IN HEALTH AND DISEASE},
	volume = {9},
	unique-id = {1406091},
	issn = {1476-511X},
	abstract = {Background and Aims: Recent studies have shown that dietary red 
		palm oil (RPO) supplementation improves functional recovery 
		following ischaemia/reperfusion in isolated hearts. The main aim 
		of this study was to investigate the effects of dietary RPO 
		supplementation on myocardial infarct size after 
		ischaemia/reperfusion injury. The effects of dietary RPO 
		supplementation on matrix metalloproteinase-2 (MMP2) activation 
		and PKB/Akt phosphorylation were also investigated. Materials 
		and methods: Male Wistar rats were divided into three groups and 
		fed a standard rat chow diet (SRC), a SRC supplemented with RPO, 
		or a SRC supplemented with sunflower oil (SFO), for a five week 
		period, respectively. After the feeding period, hearts were 
		excised and perfused on a Langendorff perfusion apparatus. 
		Hearts were subjected to thirty minutes of normothermic global 
		ischaemia and two hours of reperfusion. Infarct size was 
		determined by triphenyltetrazolium chloride staining. Coronary 
		effluent was collected for the first ten minutes of reperfusion 
		in order to measure MMP2 activity by gelatin zymography. 
		Results: Dietary RPO-supplementation decreased myocardial 
		infarct size significantly when compared to the SRC-group and 
		the SFO-supplemented group (9.1 +/- 1.0% versus 30.2 +/- 3.9% 
		and 27.1 +/- 2.4% respectively). Both dietary RPO- and SFO-
		supplementation were able to decrease MMP2 activity when 
		compared to the SRC fed group. PKB/Akt phosphorylation (Thr 308) 
		was found to be significantly higher in the dietary RPO 
		supplemented group when compared to the SFO supplemented group 
		at 10 minutes into reperfusion. There was, however, no 
		significant changes observed in ERK phosphorylation. 
		Conclusions: Dietary RPO-supplementation was found to be more 
		effective than SFO-supplementation in reducing myocardial 
		infarct size after ischaemia/reperfusion injury. Both dietary 
		RPO and SFO were able to reduce MMP2 activity, which suggests 
		that MMP2 activity does not play a major role in protection 
		offered by RPO. PKB/Akt phosphorylation may, however, be 
		involved in RPO mediated protection.},
	keywords = {Animals; Male; RATS; HEART; Rats, Wistar; Dietary Supplements; Phosphorylation/drug effects; Matrix Metalloproteinase 2/metabolism; Proto-Oncogene Proteins c-akt/metabolism; Plant Oils/*pharmacology/therapeutic use; Reperfusion Injury/diet therapy/drug therapy; Myocardial Infarction/diet therapy/*drug therapy; Dietary Fats, Unsaturated/*pharmacology/therapeutic use},
	year = {2010},
	eissn = {1476-511X},
	orcid-numbers = {Kupai, Krisztina/0000-0002-0644-1718; Csont, Tamás Bálint/0000-0001-5792-2768; Szűcs, Gergő/0000-0003-1874-2718; Csonka, Csaba/0000-0003-2532-6261; Ferdinandy, Péter/0000-0002-6424-6806}
}

@article{MTMT:1406083,
	title = {Matrix metalloproteinase activity assays: Importance of zymography},
	url = {https://m2.mtmt.hu/api/publication/1406083},
	author = {Kupai, Krisztina and Szűcs, Gergő and Cseh, Sándor and Hajdú, István and Csonka, Csaba and Csont, Tamás Bálint and Ferdinandy, Péter},
	doi = {10.1016/j.vascn.2010.02.011},
	journal-iso = {J PHARMACOL TOXICOL METH},
	journal = {JOURNAL OF PHARMACOLOGICAL AND TOXICOLOGICAL METHODS},
	volume = {61},
	unique-id = {1406083},
	issn = {1056-8719},
	abstract = {Introduction: Matrix metalloproteinases (MMPs) are zinc-dependent endopeptidases capable of degrading extracellular matrix, including the basement membrane. MMPs are associated with various physiological processes such as morphogenesis, angiogenesis, and tissue repair. Moreover, due to the novel non-matrix related intra- and extracellular targets of MMPs, dysregulation of MMP activity has been implicated in a number of acute and chronic pathological processes, such as arthritis, acute myocardial infarction, chronic heart failure, chronic obstructive pulmonary disease, inflammation, and cancer metastasis. MMPs are considered as viable drug targets in the therapy of the above diseases. Methods: For the development of selective MMP inhibitor molecules, reliable methods are necessary for target validation and lead development. Here, we discuss the major methods used for MMP assays, focusing on substrate zymography. We highlight some problems frequently encountered during sample preparations, electrophoresis, and data analysis of zymograms. Results and Discussion: Zymography is a widely used technique to study extracellular matrix-degrading enzymes, such as MMPs, from tissue extracts, cell cultures, serum or urine. This simple and sensitive technique identifies MMPs by the degradation of their substrate and by their molecular weight and therefore helps to understand the widespread role of MMPs in different pathologies and cellular pathways. (C) 2010 Elsevier Inc. All rights reserved.},
	keywords = {Animals; Humans; ARTICLE; FRET; MATRIX METALLOPROTEINASES; Enzyme-Linked Immunosorbent Assay; Molecular weight; controlled study; enzyme linked immunosorbent assay; enzyme activity; data analysis; ELECTROPHORESIS; Electrophoresis, Polyacrylamide Gel; Substrate Specificity; analytic method; enzyme degradation; Fluorescence Resonance Energy Transfer; matrix metalloproteinase; enzyme substrate; zymography; MMP inhibitors},
	year = {2010},
	eissn = {1873-488X},
	pages = {205-209},
	orcid-numbers = {Kupai, Krisztina/0000-0002-0644-1718; Szűcs, Gergő/0000-0003-1874-2718; Csonka, Csaba/0000-0003-2532-6261; Csont, Tamás Bálint/0000-0001-5792-2768; Ferdinandy, Péter/0000-0002-6424-6806}
}