@article{MTMT:34395398,
	title = {Role of the kisspeptin-KISS1R axis in the pathogenesis of chronic kidney disease and uremic cardiomyopathy},
	url = {https://m2.mtmt.hu/api/publication/34395398},
	author = {Dinh, Hoa and Kovács, Zsuzsanna and Kis, Merse and Kupecz, Klaudia and Sejben, Anita and Szűcs, Gergő and Márványkövi, Fanni and Siska, Andrea and Freiwan, Marah and Pósa, Szonja Polett and Galla, Zsolt and Ibos, Katalin Eszter and Bodnár, Éva and Lauber, Gülsüm Yilmaz and Goncalves, Ana Isabel Antunes and Acar, Eylem and Kriston, András and Kovács, Ferenc and Horváth, Péter and Bozsó, Zsolt and Tóth, Gábor and Földesi, Imre and Monostori, Péter and Cserni, Gábor and Podesser, Bruno K. and Lehoczki, Andrea Marianna and Pokreisz, Peter and Kiss, Attila and Dux, László and Csabafi, Krisztina and Sárközy, Márta},
	doi = {10.1007/s11357-023-01017-8},
	journal-iso = {GEROSCIENCE},
	journal = {GEROSCIENCE: OFFICIAL JOURNAL OF THE AMERICAN AGING ASSOCIATION (AGE)},
	volume = {46},
	unique-id = {34395398},
	issn = {2509-2715},
	abstract = {The prevalence of chronic kidney disease (CKD) is increasing globally, especially in elderly patients. Uremic cardiomyopathy is a common cardiovascular complication of CKD, characterized by left ventricular hypertrophy (LVH), diastolic dysfunction, and fibrosis. Kisspeptins and their receptor, KISS1R, exert a pivotal influence on kidney pathophysiology and modulate age-related pathologies across various organ systems. KISS1R agonists, including kisspeptin-13 (KP-13), hold promise as novel therapeutic agents within age-related biological processes and kidney-related disorders. Our investigation aimed to elucidate the impact of KP-13 on the trajectory of CKD and uremic cardiomyopathy. Male Wistar rats (300–350 g) were randomized into four groups: (I) sham-operated, (II) 5/6 nephrectomy-induced CKD, (III) CKD subjected to a low dose of KP-13 (intraperitoneal 13 µg/day), and (IV) CKD treated with a higher KP-13 dose (intraperitoneal 26 µg/day). Treatments were administered daily from week 3 for 10 days. After 13 weeks, KP-13 increased systemic blood pressure, accentuating diastolic dysfunction’s echocardiographic indicators and intensifying CKD-associated markers such as serum urea levels, glomerular hypertrophy, and tubular dilation. Notably, KP-13 did not exacerbate circulatory uremic toxin levels, renal inflammation, or fibrosis markers. In contrast, the higher KP-13 dose correlated with reduced posterior and anterior wall thickness, coupled with diminished cardiomyocyte cross-sectional areas and concurrent elevation of inflammatory ( Il6, Tnf ), fibrosis ( Col1 ), and apoptosis markers ( Bax/Bcl2 ) relative to the CKD group. In summary, KP-13’s influence on CKD and uremic cardiomyopathy encompassed heightened blood pressure and potentially activated inflammatory and apoptotic pathways in the left ventricle.},
	year = {2024},
	eissn = {2509-2723},
	pages = {2463-2488},
	orcid-numbers = {Kovács, Zsuzsanna/0000-0002-4197-4579; Sejben, Anita/0000-0002-9434-2989; Szűcs, Gergő/0000-0003-1874-2718; Márványkövi, Fanni/0000-0002-5114-1319; Pósa, Szonja Polett/0000-0002-7535-9689; Galla, Zsolt/0000-0002-9166-1212; Ibos, Katalin Eszter/0000-0001-5243-9945; Goncalves, Ana Isabel Antunes/0009-0009-3428-3321; Acar, Eylem/0000-0002-0599-6893; Kriston, András/0000-0001-8500-4315; Bozsó, Zsolt/0000-0002-5713-3096; Tóth, Gábor/0000-0002-3604-4385; Földesi, Imre/0000-0002-3329-8136; Monostori, Péter/0000-0003-3591-6054; Cserni, Gábor/0000-0003-1344-7744; Podesser, Bruno K./0000-0002-4641-7202; Lehoczki, Andrea Marianna/0000-0002-4285-7518; Pokreisz, Peter/0000-0003-2810-9000; Kiss, Attila/0000-0003-4652-1998; Dux, László/0000-0002-1270-1678; Csabafi, Krisztina/0000-0002-2008-7604; Sárközy, Márta/0000-0002-5929-2146}
}

@article{MTMT:34394136,
	title = {Chronic kidney disease may evoke anxiety by altering CRH expression in the amygdala and tryptophan metabolism in rats},
	url = {https://m2.mtmt.hu/api/publication/34394136},
	author = {Ibos, Katalin Eszter and Bodnár, Éva and Dinh, Hoa and Kis, Merse and Márványkövi, Fanni and Kovács, Zsuzsanna and Siska, Andrea and Földesi, Imre and Galla, Zsolt and Monostori, Péter and Szatmári, István and Simon, Péter and Sárközy, Márta and Csabafi, Krisztina},
	doi = {10.1007/s00424-023-02884-y},
	journal-iso = {PFLUG ARCH EUR J PHY},
	journal = {PFLUGERS ARCHIV-EUROPEAN JOURNAL OF PHYSIOLOGY},
	volume = {476},
	unique-id = {34394136},
	issn = {0031-6768},
	abstract = {Chronic kidney disease (CKD) is associated with anxiety; however, its exact mechanism is not well understood. Therefore, the aim of the present study was to assess the effect of moderate CKD on anxiety in rats. 5/6 nephrectomy was performed in male Wistar rats. 7 weeks after, anxiety-like behavior was assessed by elevated plus maze (EPM), open field (OF), and marble burying (MB) tests. At weeks 8 and 9, urinalysis was performed, and blood and amygdala samples were collected, respectively. In the amygdala, the gene expression of Avp and the gene and protein expression of Crh , Crhr1 , and Crhr2 were analyzed. Furthermore, the plasma concentration of corticosterone, uremic toxins, and tryptophan metabolites was measured by UHPLC-MS/MS. Laboratory tests confirmed the development of CKD. In the CKD group, the closed arm time increased; the central time and the total number of entries decreased in the EPM. There was a reduction in rearing, central distance and time in the OF, and fewer interactions with marbles were detected during MB. CKD evoked an upregulation of gene expression of Crh , Crhr1 , and Crhr2 , but not Avp , in the amygdala. However, there was no alteration in protein expression. In the CKD group, plasma concentrations of p-cresyl-sulfate, indoxyl-sulfate, kynurenine, kynurenic acid, 3-hydroxykynurenine, anthranilic acid, xanthurenic acid, 5-hydroxyindoleacetic acid, picolinic acid, and quinolinic acid increased. However, the levels of tryptophan, tryptamine, 5-hydroxytryptophan, serotonin, and tyrosine decreased. In conclusion, moderate CKD evoked anxiety-like behavior that might be mediated by the accumulation of uremic toxins and metabolites of the kynurenine pathway, but the contribution of the amygdalar CRH system to the development of anxiety seems to be negligible at this stage.},
	year = {2024},
	eissn = {1432-2013},
	pages = {179-196},
	orcid-numbers = {Ibos, Katalin Eszter/0000-0001-5243-9945; Dinh, Hoa/0000-0001-5812-715X; Márványkövi, Fanni/0000-0002-5114-1319; Kovács, Zsuzsanna/0000-0002-4197-4579; Földesi, Imre/0000-0002-3329-8136; Galla, Zsolt/0000-0002-9166-1212; Monostori, Péter/0000-0003-3591-6054; Szatmári, István/0000-0002-8571-5229; Sárközy, Márta/0000-0002-5929-2146; Csabafi, Krisztina/0000-0002-2008-7604}
}

@article{MTMT:34123594,
	title = {The kisspeptin-1 receptor antagonist peptide-234 aggravates uremic cardiomyopathy in a rat model},
	url = {https://m2.mtmt.hu/api/publication/34123594},
	author = {Dinh, Hoa and Kovács, Zsuzsanna and Márványkövi, Fanni and Kis, Merse and Kupecz, Klaudia and Szűcs, Gergő and Freiwan, Marah and Lauber, Gülsüm Yilmaz and Acar, Eylem and Siska, Andrea and Ibos, Katalin Eszter and Bodnár, Éva and Kriston, András and Kovács, Ferenc and Horváth, Péter and Földesi, Imre and Cserni, Gábor and Podesser, Bruno K. and Pokreisz, Peter and Kiss, Attila and Dux, László and Csabafi, Krisztina and Sárközy, Márta},
	doi = {10.1038/s41598-023-41037-0},
	journal-iso = {SCI REP},
	journal = {SCIENTIFIC REPORTS},
	volume = {13},
	unique-id = {34123594},
	issn = {2045-2322},
	abstract = {Uremic cardiomyopathy is characterized by diastolic dysfunction, left ventricular hypertrophy (LVH), and fibrosis. Dysregulation of the kisspeptin receptor (KISS1R)-mediated pathways are associated with the development of fibrosis in cancerous diseases. Here, we investigated the effects of the KISS1R antagonist peptide-234 (P234) on the development of uremic cardiomyopathy. Male Wistar rats (300–350 g) were randomized into four groups: (i) Sham, (ii) chronic kidney disease (CKD) induced by 5/6 nephrectomy, (iii) CKD treated with a lower dose of P234 ( ip. 13 µg/day), (iv) CKD treated with a higher dose of P234 ( ip. 26 µg/day). Treatments were administered daily from week 3 for 10 days. At week 13, the P234 administration did not influence the creatinine clearance and urinary protein excretion. However, the higher dose of P234 led to reduced anterior and posterior wall thicknesses, more severe interstitial fibrosis, and overexpression of genes associated with left ventricular remodeling ( Ctgf, Tgfb, Col3a1, Mmp9 ), stretch ( Nppa ), and apoptosis ( Bax, Bcl2, Casp7 ) compared to the CKD group. In contrast, no significant differences were found in the expressions of apoptosis-associated proteins between the groups. Our results suggest that the higher dose of P234 hastens the development and pathophysiology of uremic cardiomyopathy by activating the fibrotic TGF-β-mediated pathways.},
	year = {2023},
	eissn = {2045-2322},
	orcid-numbers = {Kovács, Zsuzsanna/0000-0002-4197-4579; Márványkövi, Fanni/0000-0002-5114-1319; Szűcs, Gergő/0000-0003-1874-2718; Ibos, Katalin Eszter/0000-0001-5243-9945; Földesi, Imre/0000-0002-3329-8136; Cserni, Gábor/0000-0003-1344-7744; Dux, László/0000-0002-1270-1678; Csabafi, Krisztina/0000-0002-2008-7604; Sárközy, Márta/0000-0002-5929-2146}
}

@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: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}
}

@mastersthesis{MTMT:32868192,
	title = {Comparison of the antiremodeling effects of losartan and mirabegron in a rat model of uremic cardiomyopathy [A losartan és mirabegron kezelés hatásának összehasonlítása urémiás kardiomiopátia patkány modelljében]},
	url = {https://m2.mtmt.hu/api/publication/32868192},
	author = {Kovács, Zsuzsanna},
	doi = {10.14232/phd.11064},
	publisher = {SZTE},
	unique-id = {32868192},
	year = {2021},
	orcid-numbers = {Kovács, Zsuzsanna/0000-0002-4197-4579}
}

@article{MTMT:32517976,
	title = {Investigation of the Antihypertrophic and Antifibrotic Effects of Losartan in a Rat Model of Radiation-Induced Heart Disease},
	url = {https://m2.mtmt.hu/api/publication/32517976},
	author = {Kovács, Mónika Gabriella and Kovács, Zsuzsanna and Varga, Zoltán and Szűcs, Gergő and Freiwan, Marah and Farkas, Katalin and Kővári, Bence and Cserni, Gábor and Kriston, András and Kovács, Ferenc and Horváth, Péter and Földesi, Imre and Csont, Tamás Bálint and Kahán, Zsuzsanna and Sárközy, Márta},
	doi = {10.3390/ijms222312963},
	journal-iso = {INT J MOL SCI},
	journal = {INTERNATIONAL JOURNAL OF MOLECULAR SCIENCES},
	volume = {22},
	unique-id = {32517976},
	issn = {1661-6596},
	year = {2021},
	eissn = {1422-0067},
	orcid-numbers = {Kovács, Mónika Gabriella/0000-0002-5756-4662; Kovács, Zsuzsanna/0000-0002-4197-4579; Varga, Zoltán/0000-0001-8537-6282; Szűcs, Gergő/0000-0003-1874-2718; Freiwan, Marah/0000-0002-2482-0367; Kővári, Bence/0000-0002-4498-8781; Cserni, Gábor/0000-0003-1344-7744; Földesi, Imre/0000-0002-3329-8136; Csont, Tamás Bálint/0000-0001-5792-2768; Kahán, Zsuzsanna/0000-0002-5021-8775; Sárközy, Márta/0000-0002-5929-2146}
}

@article{MTMT:32191180,
	title = {Ischemic preconditioning protects the heart against ischemia-reperfusion injury in chronic kidney disease in both males and females},
	url = {https://m2.mtmt.hu/api/publication/32191180},
	author = {Sárközy, Márta and Márványkövi, Fanni and Szűcs, Gergő and Kovács, Zsuzsanna and Szabó, Márton Richárd and Molnár-Gáspár, Renáta and Siska, Andrea and Kővári, Bence and Cserni, Gábor and Földesi, Imre and Csont, Tamás Bálint},
	doi = {10.1186/s13293-021-00392-1},
	journal-iso = {BIOL SEX DIFFER},
	journal = {BIOLOGY OF SEX DIFFERENCES},
	volume = {12},
	unique-id = {32191180},
	year = {2021},
	eissn = {2042-6410},
	orcid-numbers = {Sárközy, Márta/0000-0002-5929-2146; Márványkövi, Fanni/0000-0002-5114-1319; Szűcs, Gergő/0000-0003-1874-2718; Kovács, Zsuzsanna/0000-0002-4197-4579; Szabó, Márton Richárd/0000-0003-0415-5192; Molnár-Gáspár, Renáta/0000-0001-9673-4532; Kővári, Bence/0000-0002-4498-8781; Cserni, Gábor/0000-0003-1344-7744; Földesi, Imre/0000-0002-3329-8136; Csont, Tamás Bálint/0000-0001-5792-2768}
}

@article{MTMT:32172362,
	title = {Comparison of the antiremodeling effects of losartan and mirabegron in a rat model of uremic cardiomyopathy},
	url = {https://m2.mtmt.hu/api/publication/32172362},
	author = {Kovács, Zsuzsanna and Szűcs, Gergő and Freiwan, Marah and Kovács, Mónika Gabriella and Márványkövi, Fanni and Dinh, Hoa and Siska, Andrea and Farkas, Katalin and Kovács, Ferenc and Kriston, András and Horváth, Péter and Kővári, Bence and Cserni, Bálint Gábor and Cserni, Gábor and Földesi, Imre and Csont, Tamás Bálint and Sárközy, Márta},
	doi = {10.1038/s41598-021-96815-5},
	journal-iso = {SCI REP},
	journal = {SCIENTIFIC REPORTS},
	volume = {11},
	unique-id = {32172362},
	issn = {2045-2322},
	year = {2021},
	eissn = {2045-2322},
	orcid-numbers = {Kovács, Zsuzsanna/0000-0002-4197-4579; Szűcs, Gergő/0000-0003-1874-2718; Kovács, Mónika Gabriella/0000-0002-5756-4662; Márványkövi, Fanni/0000-0002-5114-1319; Kővári, Bence/0000-0002-4498-8781; Cserni, Gábor/0000-0003-1344-7744; Földesi, Imre/0000-0002-3329-8136; Csont, Tamás Bálint/0000-0001-5792-2768; Sárközy, Márta/0000-0002-5929-2146}
}

@article{MTMT:31877554,
	title = {Pathomechanisms and therapeutic opportunities in radiation‑induced heart disease: from bench to bedside},
	url = {https://m2.mtmt.hu/api/publication/31877554},
	author = {Sárközy, Márta and Varga, Zoltán and Molnár-Gáspár, Renáta and Szűcs, Gergő and Kovács, Mónika Gabriella and Kovács, Zsuzsanna and Dux, László and Kahán, Zsuzsanna and Csont, Tamás Bálint},
	doi = {10.1007/s00392-021-01809-y},
	journal-iso = {CLIN RES CARDIOL},
	journal = {CLINICAL RESEARCH IN CARDIOLOGY},
	volume = {110},
	unique-id = {31877554},
	issn = {1861-0684},
	year = {2021},
	eissn = {1861-0692},
	pages = {507-531},
	orcid-numbers = {Sárközy, Márta/0000-0002-5929-2146; Varga, Zoltán/0000-0001-8537-6282; Molnár-Gáspár, Renáta/0000-0001-9673-4532; Szűcs, Gergő/0000-0003-1874-2718; Kovács, Mónika Gabriella/0000-0002-5756-4662; Kovács, Zsuzsanna/0000-0002-4197-4579; Dux, László/0000-0002-1270-1678; Kahán, Zsuzsanna/0000-0002-5021-8775; Csont, Tamás Bálint/0000-0001-5792-2768}
}