@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}
}

@mastersthesis{MTMT:34126375,
	title = {Investigation of the pathomechanism of uremic cardiomyopathy and the infarctsize-limiting effect of ischemic preconditioning in a rat model of chronic kidney disease [Az urémiás kardiomiopátia és a szív iszkémiás prekondícionálhatóságának vizsgálata krónikus veseelégtelenségben patkány modellben]},
	url = {https://m2.mtmt.hu/api/publication/34126375},
	author = {Márványkövi, Fanni},
	doi = {10.14232/phd.11611},
	publisher = {Universití of Szeged},
	unique-id = {34126375},
	abstract = {Chronic kidney disease (CKD) is a public health problem affecting 1 of 10people worldwide. Interestingly, approximately 60% of patients are women in theearly stages of CKD. A common cardiovascular complication of CKD is uremiccardiomyopathy, most characterized by left ventricular hypertrophy (LVH) andfibrosis, ultimately leading to heart failure (HF). Moreover, uremiccardiomyopathy enhances the susceptibility of the heart to acute myocardialinfarction (AMI). However, the precise molecular mechanisms and the role ofsex-based differences in the development of uremic cardiomyopathy and AMI in CKDare still unclear. Therefore, novel therapeutic strategies that alleviate theseverity of uremic cardiomyopathy and AMI in CKD are urgently needed.MicroRNA-212 (miR-212) has been demonstrated previously to be a crucialregulator of pathologic LVH in pressure-overload-induced HF via regulating theforkhead box O3 (FOXO3)/calcineurin/nuclear factor of activated T-cells (NFAT)pathway. Here we aimed to investigate whether i) miR-212 and its selectedhypertrophy- and fibrosis-associated targets play a role in the development ofuremic cardiomyopathy, ii) the influence of sex on the severity of uremiccardiomyopathy and AMI, as well as the infarct size-limiting effect of ischemicpreconditioning (IPRE) in experimental CKD. CKD was induced by 5/6 nephrectomyin male and female Wistar rats. Serum and urine laboratory parameters weremeasured to verify the development of CKD 8 or 9 weeks after the operations.Transthoracic echocardiography was performed to assess cardiac function andmorphology. Cardiomyocyte hypertrophy and fibrosis were measured by histology.Left ventricular (LV) samples were collected for RT-qPCR, Western blot, andELISA measurements. The LV expressions of miR-212 and its LVH andfibrosis-associated selected targets, including FOXO3, AKT, and ERK1/2, weremeasured only in males by RT-qPCR and/or Western blot. In a subgroup of animals,hearts were perfused according to Langendorf and were subjected to 35 min globalischemia and 120 min reperfusion with or without IPRE. Then the infarct size orphosphorylated (p) and total forms of proteins related to the cardioprotectiveRISK (AKT, ERK1/2) and SAFE (STAT3) pathways were measured in the myocardialsamples by Western blot. The severity of CKD was similar in males and femalesbased on serum urea and creatinine levels. In CKD, diastolic dysfunctiondeveloped with preserved ejection fraction and increased A-type natriureticpeptide (ANP) levels in both sexes; however, males developed more severe LVHthan females. Moreover, histology showed the development of marked cardiacfibrosis only in CKD in males. The miR-212 was significantly overexpressed inthe LV samples in CKD in males. However, the LV expression of FOXO3, AMPK, andERK1/2 failed to change significantly at the mRNA or protein level.Interestingly, only the LV pAKT/AKT ratio was significantly increased in malesin CKD. Females had significantly smaller infarct sizes both in the sham and CKDgroups compared to males. In both sexes, IPRE significantly decreased theinfarct size in both the sham-operated and CKD groups. IPRE significantlyincreased the pSTAT3/STAT3 ratio in sham-operated but not in CKD animals in bothsexes. The groups had no significant differences in pAKT/AKT and pERK1/2 /ERK1/2 ratios. In summary, cardiac overexpression of miR-212 in CKD failed toaffect its previously implicated hypertrophy- and fibrosis-associated downstreamtargets in males. Thus, the molecular mechanism of the development of LVH in CKDseems to be independent of the FOXO3, ERK1/2, and AMPK in our model. The infarctsize-limiting effect of IPRE was preserved in both sexes in CKD despite the moresevere uremic cardiomyopathy in male CKD rats and the smaller infarct size infemales. Further research is needed to identify crucial molecular mechanisms inthe development of uremic cardiomyopathy and the cardioprotective effects ofIPRE in CKD.},
	year = {2023},
	orcid-numbers = {Márványkövi, Fanni/0000-0002-5114-1319}
}

@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: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:31289428,
	title = {A nemi különbségek hatása a szív iszkémiás prekondícionálhatóságára krónikus veseelégtelenségben [The effect of gender differences on cardiac ischemic preconditioning in chronic kidney disease]},
	url = {https://m2.mtmt.hu/api/publication/31289428},
	author = {Sárközy, Márta and Márványkövi, Fanni and Szűcs, Gergő and Molnár-Gáspár, Renáta and Dajka, Dalma and Siska, Andrea and Földesi, Imre and Csont, Tamás Bálint},
	journal-iso = {CARDIOL HUNG},
	journal = {CARDIOLOGIA HUNGARICA},
	volume = {49},
	unique-id = {31289428},
	issn = {0133-5596},
	year = {2019},
	eissn = {1588-0230},
	pages = {B32-B33},
	orcid-numbers = {Sárközy, Márta/0000-0002-5929-2146; Márványkövi, Fanni/0000-0002-5114-1319; Szűcs, Gergő/0000-0003-1874-2718; Molnár-Gáspár, Renáta/0000-0001-9673-4532; Földesi, Imre/0000-0002-3329-8136; Csont, Tamás Bálint/0000-0001-5792-2768}
}

@{MTMT:31289422,
	title = {Krónikus veseelégtelenségben megemelkedik a prohipertrófiás miR-212 bal kamrai expressziója},
	url = {https://m2.mtmt.hu/api/publication/31289422},
	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},
	booktitle = {FAMÉ 2019 Magyar Kísérletes és Klinikai Farmakológiai Társaság; Magyar Anatómus Társaság; Magyar Mikrocirkulációs és Vaszkuláris Biológiai Társaság; Magyar Élettani Társaság},
	unique-id = {31289422},
	year = {2019},
	pages = {107-108},
	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; Csont, Tamás Bálint/0000-0001-5792-2768}
}

@misc{MTMT:31289397,
	title = {Chronic kidney disease induces left ventricular overexpression of the pro-hypertrophic microRNA-212},
	url = {https://m2.mtmt.hu/api/publication/31289397},
	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, L ászló and Földesi, Imre and Thum, Thomas and Bátkai, Sándor and Csont, Tamás Bálint},
	unique-id = {31289397},
	year = {2019},
	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; Csont, Tamás Bálint/0000-0001-5792-2768}
}