@article{MTMT:34416566,
	title = {Triptofán-származékok, mint lehetséges biomarkerek és terápiás célpontok egyes kardiovaszkuláris megbetegedésekben [Tryptophan metabolites as potential biomarkers and therapeutic targets in certain cardiovascular diseases]},
	url = {https://m2.mtmt.hu/api/publication/34416566},
	author = {Nógrádi-Halmi, Dóra and Erdélyi-Furka, Barbara Fanni and Molnár-Gáspár, Renáta and Csont, Tamás Bálint},
	doi = {10.26430/CHUNGARICA.2023.53.5.468},
	journal-iso = {CARDIOL HUNG},
	journal = {CARDIOLOGIA HUNGARICA},
	volume = {53},
	unique-id = {34416566},
	issn = {0133-5596},
	abstract = {A gyulladásos folyamatok kiemelkedő szereppel bírnak a vezető halálokok közé sorolható koszorúér-betegségek patomechanizmusában és progressziójában. Ismert, hogy az ezen folyamatok során felszabaduló proinflammatorikus molekulák képesek elősegíteni a triptofán-aminosav kinurenin-útvonalon történő lebomlását. Ez számos immunmodulátor kinurenin-metabolit felszabadulását teszi lehetővé, amelyek között egyaránt szerepelnek jótékony, valamint káros hatással bíró vegyületek. Mai tudásunk szerint a különböző kinurenin-származékok előállításáért felelős metabolikus útvonalak egyensúlyának felborulása fontos szereppel bírhat bizonyos betegségek, köztük egyes kardiovaszkuláris megbetegedések kórlefolyásában. Több tanulmány is alátámasztja, hogy számos kinurenin-metabolit koncentrációjának változása kimutatható koszorúér-betegségben szenvedő páciensektől nyert vér- és/vagy vizeletmintákban. Egyes közlemények szerint bizonyos kinureninek szérumszintje korrelálhat a koronáriabetegségek progressziójával. Összefoglaló tanulmányunk célja annak áttekintése, hogy a kinureninek szereppel bírhatnak-e a jövőben egyes kardiovaszkuláris betegségek rizikóbecslésében, mint biomarkerek, illetve segíthetik-e új terápiás stratégiák kidolgozását.},
	year = {2023},
	eissn = {1588-0230},
	pages = {468-475},
	orcid-numbers = {Nógrádi-Halmi, Dóra/0000-0001-9496-9354; Erdélyi-Furka, Barbara Fanni/0009-0005-7805-1910; Molnár-Gáspár, Renáta/0000-0001-9673-4532; Csont, Tamás Bálint/0000-0001-5792-2768}
}

@article{MTMT:34416562,
	title = {Piroptózis, PANoptózis és ferroptózis a szív iszkémia/reperfúziós károsodásában},
	url = {https://m2.mtmt.hu/api/publication/34416562},
	author = {Pipicz, Márton and Demján, Virág and Csonka, Csaba and Csont, Tamás Bálint},
	doi = {10.26430/CHUNGARICA.2023.53.5.451},
	journal-iso = {CARDIOL HUNG},
	journal = {CARDIOLOGIA HUNGARICA},
	volume = {53},
	unique-id = {34416562},
	issn = {0133-5596},
	abstract = {Az intenzív kutatások ellenére továbbra sem rendelkezünk olyan kardioprotektív gyógyszerekkel, amelyek a szív iszkémia/reperfúziós (I/R) károsodásával járó infarktusméretet hatásosan csökkentenék. Ennek egyik magyarázata, hogy az I/R-t kísérő sejtelhalás összetett folyamata teljesen még nem tisztázott. A mechanizmus részletesebb megismerése javíthatja a kardioprotektív gyógyszerfejlesztések transzlálhatóságát. A klasszikus szabályozott (apoptózis, autofágia-mediálta sejthalál) és nem szabályozott (nekrózis) sejthalálfolyamatok mellett olyan programozott sejthalálformákat és mechanizmusokat ismertünk meg az elmúlt években, mint például a piroptózis, a PANoptózis vagy a ferroptózis. Jelen összefoglaló közleményünkben ezen folyamatokat kívánjuk röviden bemutatni a szív I/R károsodásában, valamint kitérünk a lehetséges modulálási stratégiákra is.},
	year = {2023},
	eissn = {1588-0230},
	pages = {451-458},
	orcid-numbers = {Pipicz, Márton/0000-0002-0944-1684; Demján, Virág/0000-0002-6792-3024; Csonka, Csaba/0000-0003-2532-6261; Csont, Tamás Bálint/0000-0001-5792-2768}
}

@article{MTMT:34167864,
	title = {Effect of Eccentric Exercise on Metabolic Health in Diabetes and Obesity},
	url = {https://m2.mtmt.hu/api/publication/34167864},
	author = {Szűcs, Gergő and Pipicz, Márton and Szabó, Márton Richárd and Csont, Tamás Bálint and Török, László and Csonka, Csaba},
	doi = {10.1186/s40798-023-00596-2},
	journal-iso = {SPORT MED-OPEN},
	journal = {SPORTS MEDICINE-OPEN},
	volume = {9},
	unique-id = {34167864},
	issn = {2199-1170},
	abstract = {There is a growing body of evidence showing the importance of physical activity against civilization-induced metabolic diseases, including type 2 diabetes (T2DM) and obesity. Eccentric contraction, when skeletal muscles generate force by lengthening, is a unique type of skeletal muscle activity. Eccentric contraction may lead to better power production characteristics of the muscle because eccentric contraction requires less energy and can result in higher tension. Therefore, it is an ideal tool in the rehabilitation program of patients. However, the complex metabolic effect (i.e., fat mass reduction, increased lipid oxidation, improvement in blood lipid profile, and increased insulin sensitivity) of the eccentric contraction alone has scarcely been investigated. This paper aims to review the current literature to provide information on whether eccentric contraction can influence metabolic health and body composition in T2DM or obesity. We also discussed the potential role of myokines in mediating the effects of eccentric exercise. A better understanding of the mechanism of eccentric training and particularly their participation in the regulation of metabolic diseases may widen their possible therapeutic use and, thereby, may support the fight against the leading global risks for mortality in the world.},
	year = {2023},
	eissn = {2198-9761},
	orcid-numbers = {Szűcs, Gergő/0000-0003-1874-2718; Pipicz, Márton/0000-0002-0944-1684; Szabó, Márton Richárd/0000-0003-0415-5192; Csont, Tamás Bálint/0000-0001-5792-2768; Csonka, Csaba/0000-0003-2532-6261}
}

@article{MTMT:34008336,
	title = {The effect of electrical stimulation of skeletal muscle on cardioprotection and on muscle-derived myokine levels in rats: A pilot study},
	url = {https://m2.mtmt.hu/api/publication/34008336},
	author = {Szabó, Márton Richárd and Csont, Tamás Bálint and Csonka, Csaba},
	doi = {10.1556/2060.2023.00198},
	journal-iso = {PHYSIOL INT},
	journal = {PHYSIOLOGY INTERNATIONAL},
	volume = {110},
	unique-id = {34008336},
	issn = {2498-602X},
	abstract = {Electrical muscle stimulation (EMS) is a widely used method in sports and rehabilitation therapies to simulate physical exercise. EMS treatment via skeletal muscle activity improves the cardiovascular functions and the overall physical condition of the patients. However, the cardioprotective effect of EMS has not been proven so far, therefore, the aim of this study was to investigate the potential cardiac conditioning effect of EMS in an animal model. Low-frequency 35-min EMS was applied to the gastrocnemius muscle of male Wistar rats for three consecutive days. Their isolated hearts were then subjected to 30 min global ischemia and 120 min reperfusion. At the end of reperfusion cardiac specific creatine kinase (CK-MB) and lactate dehydrogenase (LDH) enzyme release and myocardial infarct size were determined. Additionally, skeletal muscle-driven myokine expression and release were also assessed. Phosphorylation of cardioprotective signaling pathway members AKT, ERK1/2, and STAT3 proteins were also measured. EMS significantly attenuated cardiac LDH and CK-MB enzyme activities in the coronary effluents at the end of the ex vivo reperfusion. EMS treatment considerably altered the myokine content of the stimulated gastrocnemius muscle without altering circulating myokine levels in the serum. Additionally, phosphorylation of cardiac AKT, ERK1/2, and STAT3 was not significantly different in the two groups. Despite the lack of significant infarct size reduction, the EMS treatment seems to influence the course of cellular damage due to ischemia/reperfusion and favorably modifies skeletal muscle myokine expressions. Our results suggest that EMS may have a protective effect on the myocardium, however, further optimization is required.},
	year = {2023},
	eissn = {2677-0164},
	pages = {135-149},
	orcid-numbers = {Szabó, Márton Richárd/0000-0003-0415-5192; Csont, Tamás Bálint/0000-0001-5792-2768; Csonka, Csaba/0000-0003-2532-6261}
}

@article{MTMT:33941648,
	title = {Neuregulin-1β Improves Uremic Cardiomyopathy and Renal Dysfunction in Rats},
	url = {https://m2.mtmt.hu/api/publication/33941648},
	author = {Sárközy, Márta and Watzinger, Simon and Kovács, Zsuzsanna and Acar, Eylem and Márványkövi, Fanni and Szűcs, Gergő and Lauber, Gülsüm Yilmaz and Galla, Zsolt and Siska, Andrea and Földesi, Imre and Fintha, Attila and Kriston, András and Kovács, Ferenc and Horváth, Péter and Kővári, Bence and Cserni, Gábor and Krenács, Tibor and Szabó, Petra Lujza and Szabó, Gábor Tamás and Monostori, Péter and Zins, Karin and Abraham, Dietmar and Csont, Tamás Bálint and Pokreisz, Peter and Podesser, Bruno K. and Kiss, Attila},
	doi = {10.1016/j.jacbts.2023.03.003},
	journal-iso = {JACC-BASIC TRANSL SC},
	journal = {JACC:BASIC TO TRANSLATIONAL SCIENCE},
	volume = {8},
	unique-id = {33941648},
	issn = {2452-302X},
	year = {2023},
	eissn = {2452-302X},
	pages = {1160-1176},
	orcid-numbers = {Sárközy, Márta/0000-0002-5929-2146; Kovács, Zsuzsanna/0000-0002-4197-4579; Márványkövi, Fanni/0000-0002-5114-1319; Szűcs, Gergő/0000-0003-1874-2718; Galla, Zsolt/0000-0002-9166-1212; Földesi, Imre/0000-0002-3329-8136; Fintha, Attila/0000-0002-0519-8170; Kővári, Bence/0000-0002-4498-8781; Cserni, Gábor/0000-0003-1344-7744; Krenács, Tibor/0000-0001-9164-065X; Monostori, Péter/0000-0003-3591-6054; Csont, Tamás Bálint/0000-0001-5792-2768; Pokreisz, Peter/0000-0003-2810-9000}
}

@article{MTMT:33322061,
	title = {Acetylation State of Lysine 14 of Histone H3.3 Affects Mutant Huntingtin Induced Pathogenesis},
	url = {https://m2.mtmt.hu/api/publication/33322061},
	author = {Faragó, Anikó and Zsindely, Nóra and Farkas, Anita and Neller, Alexandra and Siági, Fruzsina and Szabó, Márton Richárd and Csont, Tamás Bálint and Bodai, László},
	doi = {10.3390/ijms232315173},
	journal-iso = {INT J MOL SCI},
	journal = {INTERNATIONAL JOURNAL OF MOLECULAR SCIENCES},
	volume = {23},
	unique-id = {33322061},
	issn = {1661-6596},
	abstract = {Huntington’s Disease (HD) is a fatal neurodegenerative disorder caused by the expansion of a polyglutamine-coding CAG repeat in the Huntingtin gene. One of the main causes of neurodegeneration in HD is transcriptional dysregulation that, in part, is caused by the inhibition of histone acetyltransferase (HAT) enzymes. HD pathology can be alleviated by increasing the activity of specific HATs or by inhibiting histone deacetylase (HDAC) enzymes. To determine which histone’s post-translational modifications (PTMs) might play crucial roles in HD pathology, we investigated the phenotype-modifying effects of PTM mimetic mutations of variant histone H3.3 in a Drosophila model of HD. Specifically, we studied the mutations (K→Q: acetylated; K→R: non-modified; and K→M: methylated) of lysine residues K9, K14, and K27 of transgenic H3.3. In the case of H3.3K14Q modification, we observed the amelioration of all tested phenotypes (viability, longevity, neurodegeneration, motor activity, and circadian rhythm defects), while H3.3K14R had the opposite effect. H3.3K14Q expression prevented the negative effects of reduced Gcn5 (a HAT acting on H3K14) on HD pathology, while it only partially hindered the positive effects of heterozygous Sirt1 (an HDAC acting on H3K14). Thus, we conclude that the Gcn5-dependent acetylation of H3.3K14 might be an important epigenetic contributor to HD pathology.},
	year = {2022},
	eissn = {1422-0067},
	orcid-numbers = {Zsindely, Nóra/0000-0002-6189-3100; Szabó, Márton Richárd/0000-0003-0415-5192; Csont, Tamás Bálint/0000-0001-5792-2768; Bodai, László/0000-0001-8411-626X}
}

@{MTMT:33104875,
	title = {The cytoprotective effect of kynurenic acid against simulated ischemia/reoxygenation-induced damage of cardiac cells},
	url = {https://m2.mtmt.hu/api/publication/33104875},
	author = {Nógrádi-Halmi, Dóra and Molnár-Gáspár, Renáta and Csontné Kiricsi, Mónika and Nóra, Igaz and Csont, Tamás Bálint},
	booktitle = {Abstract book of Annual Meeting of the Hungarian Biochemical Society 2022},
	unique-id = {33104875},
	year = {2022},
	pages = {91},
	orcid-numbers = {Nógrádi-Halmi, Dóra/0000-0001-9496-9354; Molnár-Gáspár, Renáta/0000-0001-9673-4532; Csontné Kiricsi, Mónika/0000-0002-8416-2052; Csont, Tamás Bálint/0000-0001-5792-2768}
}

@{MTMT:33032074,
	title = {MicroRNA-based therapeutic strategies for chronic kidney disease and uremic cardiomyopathy [Chapter 28]},
	url = {https://m2.mtmt.hu/api/publication/33032074},
	author = {Sárközy, Márta and Csont, Tamás Bálint},
	booktitle = {MicroRNA},
	doi = {10.1016/B978-0-323-89774-7.00006-6},
	unique-id = {33032074},
	year = {2022},
	pages = {563-600},
	orcid-numbers = {Sárközy, Márta/0000-0002-5929-2146; Csont, Tamás Bálint/0000-0001-5792-2768}
}

@article{MTMT:32924828,
	title = {Diet-Induced Hypercholesterolemia Leads to Cardiac Dysfunction and Alterations in the Myocardial Proteome},
	url = {https://m2.mtmt.hu/api/publication/32924828},
	author = {Szabó, Márton Richárd and Pipicz, Márton and Sárközy, Márta and Bruszel, Bella and Szabó, Zoltán and Csont, Tamás Bálint},
	doi = {10.3390/ijms23137387},
	journal-iso = {INT J MOL SCI},
	journal = {INTERNATIONAL JOURNAL OF MOLECULAR SCIENCES},
	volume = {23},
	unique-id = {32924828},
	issn = {1661-6596},
	abstract = {Elevated blood cholesterol is a major risk factor for coronary heart disease. Moreover, direct effects on the myocardium also contribute to the adverse effects of hypercholesterolemia. Here, we investigated the effect of hypercholesterolemia on the cardiac proteome. Male Wistar rats were fed with a laboratory rodent chow supplemented with 2% cholesterol for 8 weeks to induce hypercholesterolemia. The protein expression data obtained from the proteomic characterization of left ventricular samples from normo- and hypercholesterolemic animals were subjected to gene ontology (GO) and protein interaction analyses. Elevated circulating cholesterol levels were accompanied by diastolic dysfunction in cholesterol-fed rats. The proteomic characterization of left ventricular samples revealed altered expression of 45 proteins due to hypercholesterolemia. Based on the Gene Ontology analysis, hypercholesterolemia was associated with disturbed expression of cytoskeletal and contractile proteins. Beta-actin was downregulated in the hypercholesterolemic myocardium, and established a prominent hub of the protein interaction network. Analysis of the unfiltered dataset revealed concordant downregulated expression patterns in proteins associated with the arrangement of the contractile system (e.g., cardiac-specific troponins and myosin complex), and in subunits of the mitochondrial respiratory chain. We conclude that the observed changes in the cardiac proteome may contribute to the development of diastolic dysfunction in hypercholesterolemia.},
	year = {2022},
	eissn = {1422-0067},
	orcid-numbers = {Szabó, Márton Richárd/0000-0003-0415-5192; Pipicz, Márton/0000-0002-0944-1684; Sárközy, Márta/0000-0002-5929-2146; Szabó, Zoltán/0000-0001-8278-8038; Csont, Tamás Bálint/0000-0001-5792-2768}
}

@article{MTMT:32689754,
	title = {Investigation of the Antiremodeling Effects of Losartan, Mirabegron and Their Combination on the Development of Doxorubicin-Induced Chronic Cardiotoxicity in a Rat Model},
	url = {https://m2.mtmt.hu/api/publication/32689754},
	author = {Freiwan, Marah and Kovács, Mónika Gabriella and Kovács, Zsuzsanna and Szűcs, Gergő and Dinh, Hoa and Losonczi, Réka Hajnalka and Siska, Andrea and Kriston, András and Kovács, Ferenc and Horváth, Péter and Földesi, Imre and Cserni, Gábor and Dux, László and Csont, Tamás Bálint and Sárközy, Márta},
	doi = {10.3390/ijms23042201},
	journal-iso = {INT J MOL SCI},
	journal = {INTERNATIONAL JOURNAL OF MOLECULAR SCIENCES},
	volume = {23},
	unique-id = {32689754},
	issn = {1661-6596},
	abstract = {Despite the effectiveness of doxorubicin (DOXO) as a chemotherapeutic agent, dose-dependent development of chronic cardiotoxicity limits its application. The angiotensin-II receptor blocker losartan is commonly used to treat cardiac remodeling of various etiologies. The beta-3 adrenergic receptor agonist mirabegron was reported to improve chronic heart failure. Here we investigated the effects of losartan, mirabegron and their combination on the development of DOXO-induced chronic cardiotoxicity. Male Wistar rats were divided into five groups: (i) control; (ii) DOXO-only; (iii) losartan-treated DOXO; (iv) mirabegron-treated DOXO; (v) losartan plus mirabegron-treated DOXO groups. The treatments started 5 weeks after DOXO administration. At week 8, echocardiography was performed. At week 9, left ventricles were prepared for histology, qRT-PCR, and Western blot measurements. Losartan improved diastolic but not systolic dysfunction and ameliorated SERCA2a repression in our DOXO-induced cardiotoxicity model. The DOXO-induced overexpression of Il1 and Il6 was markedly decreased by losartan and mirabegron. Mirabegron and the combination treatment improved systolic and diastolic dysfunction and significantly decreased overexpression of Smad2 and Smad3 in our DOXO-induced cardiotoxicity model. Only mirabegron reduced DOXO-induced cardiac fibrosis significantly. Mirabegron and its combination with losartan seem to be promising therapeutic tools against DOXO-induced chronic cardiotoxicity.},
	keywords = {heart failure; diastolic dysfunction; Cardiac fibrosis; angiotensin II receptor blocker; cardiac inflammation; TGF-beta/SMAD signaling pathway; Onco-cardiology; doxorubicin-induced chronic cardiotoxicity; beta-3 adrenoceptor agonist; sarcoendoplasmic reticulum calcium ATPase 2a},
	year = {2022},
	eissn = {1422-0067},
	orcid-numbers = {Freiwan, Marah/0000-0002-2482-0367; Kovács, Mónika Gabriella/0000-0002-5756-4662; Kovács, Zsuzsanna/0000-0002-4197-4579; Szűcs, Gergő/0000-0003-1874-2718; Losonczi, Réka Hajnalka/0009-0001-7220-2184; Földesi, Imre/0000-0002-3329-8136; Cserni, Gábor/0000-0003-1344-7744; Dux, László/0000-0002-1270-1678; Csont, Tamás Bálint/0000-0001-5792-2768; Sárközy, Márta/0000-0002-5929-2146}
}