@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}
}

@book{MTMT:34446677,
	title = {2023. évi Orvos- és Egészségtudományi TDK Konferencia},
	url = {https://m2.mtmt.hu/api/publication/34446677},
	isbn = {9789633069592},
	editor = {Tolnai, József and Peták, Ferenc and Fodor, Gergely and Rakonczay, Zoltán},
	publisher = {Universití of Szeged},
	unique-id = {34446677},
	year = {2023},
	orcid-numbers = {Tolnai, József/0000-0002-7648-764X; Peták, Ferenc/0000-0001-6249-9327; Fodor, Gergely/0000-0002-4736-4966; Rakonczay, Zoltán/0000-0002-1499-3416}
}

@article{MTMT:34193757,
	title = {A Brain Region-Dependent Alteration in the Expression of Vasopressin, Corticotropin-Releasing Factor, and Their Receptors Might Be in the Background of Kisspeptin-13-Induced Hypothalamic-Pituitary-Adrenal Axis Activation and Anxiety in Rats},
	url = {https://m2.mtmt.hu/api/publication/34193757},
	author = {Csabafi, Krisztina and Ibos, Katalin Eszter and Bodnár, Éva and Filkor, Kata and Szakács, Júlia and Bagosi, Zsolt},
	doi = {10.3390/biomedicines11092446},
	journal-iso = {BIOMEDICINES},
	journal = {BIOMEDICINES},
	volume = {11},
	unique-id = {34193757},
	abstract = {Previously, we reported that intracerebroventricularly administered kisspeptin-13 (KP-13) induces anxiety-like behavior and activates the hypothalamic-pituitary-adrenal (HPA) axis in rats. In the present study, we aimed to shed light on the mediation of KP-13′s stress-evoking actions. The relative gene expressions of the corticotropin-releasing factor (Crf, Crfr1, and Crfr2) and arginine vasopressin (Avp, Avpr1a, and Avpr1b) systems were measured in the amygdala and hippocampus of male Wistar rats after icv KP-13 treatment. CRF and AVP protein content were also determined. A different set of animals received CRF or V1 receptor antagonist pretreatment before the KP-13 challenge, after which either an open-field test or plasma corticosterone levels measurement was performed. In the amygdala, KP-13 induced an upregulation of Avp and Avpr1b expression, and a downregulation of Crf. In the hippocampus, the mRNA level of Crf increased and the level of Avpr1a decreased. A significant rise in AVP protein content was also detected in the amygdala. KP-13 also evoked anxiety-like behavior in the open field test, which the V1 receptor blocker antagonized. Both CRF and V1 receptor blockers reduced the KP-13-evoked rise in the plasma corticosterone level. This suggests that KP-13 alters the AVP and CRF signaling and that might be responsible for its effect on the HPA axis and anxiety-like behavior.},
	year = {2023},
	eissn = {2227-9059},
	orcid-numbers = {Csabafi, Krisztina/0000-0002-2008-7604; Ibos, Katalin Eszter/0000-0001-5243-9945}
}

@article{MTMT:34189729,
	title = {Ghrelin Amplifies the Nicotine-Induced Release of Dopamine in the Bed Nucleus of Stria Terminalis (BNST)},
	url = {https://m2.mtmt.hu/api/publication/34189729},
	author = {Ayman, Jázmin and Palotai, M. and Dochnal, Roberta and Bagosi, Zsolt},
	doi = {10.3390/biomedicines11092456},
	journal-iso = {BIOMEDICINES},
	journal = {BIOMEDICINES},
	volume = {11},
	unique-id = {34189729},
	year = {2023},
	eissn = {2227-9059}
}

@article{MTMT:34183455,
	title = {The anti-inflammatory effect of dimethyl trisulfide in experimental acute pancreatitis},
	url = {https://m2.mtmt.hu/api/publication/34183455},
	author = {Orján, Erik Márk and Kormányos, Eszter Sára and Fűr, Gabriella and Dombi, Ágnes and Bálint, Emese Réka and Balla, Zsolt and Balog, Beáta Adél and Dágó, Ágnes and Totonji, Ahmad and Bátai, István Zoárd and Jurányi, Eszter Petra and Ditrói, Tamás and Al-omari, Ammar and Pozsgai, Gábor and Kormos, Viktória and Nagy, Péter and Pintér, Erika and Rakonczay, Zoltán and Kiss, Lóránd},
	doi = {10.1038/s41598-023-43692-9},
	journal-iso = {SCI REP},
	journal = {SCIENTIFIC REPORTS},
	volume = {13},
	unique-id = {34183455},
	issn = {2045-2322},
	abstract = {Various organosulfur compounds, such as dimethyl trisulfide (DMTS), display anti-inflammatory properties. We aimed to examine the effects of DMTS on acute pancreatitis (AP) and its mechanism of action in both in vivo and in vitro studies. AP was induced in FVB/n mice or Wistar rats by caerulein, ethanol-palmitoleic acid, or L-ornithine-HCl. DMTS treatments were administered subcutaneously. AP severity was assessed by pancreatic histological scoring, pancreatic water content, and myeloperoxidase activity measurements. The behaviour of animals was followed. Pancreatic heat shock protein 72 (HSP72) expression, sulfide, and protein persulfidation were measured. In vitro acinar viability, intracellular Ca 2+ concentration, and reactive oxygen species production were determined. DMTS dose-dependently decreased the severity of AP. It declined the pancreatic infiltration of leukocytes and cellular damage in mice. DMTS upregulated the HSP72 expression during AP and elevated serum sulfide and low molecular weight persulfide levels. DMTS exhibited cytoprotection against hydrogen peroxide and AP-inducing agents. It has antioxidant properties and modulates physiological but not pathophysiological Ca 2+ signalling. Generally, DMTS ameliorated AP severity and protected pancreatic acinar cells. Our findings indicate that DMTS is a sulfur donor with anti-inflammatory and antioxidant effects, and organosulfur compounds require further investigation into this potentially lethal disease.},
	year = {2023},
	eissn = {2045-2322},
	orcid-numbers = {Orján, Erik Márk/0000-0003-4176-0834; Balog, Beáta Adél/0009-0008-3568-4090; Jurányi, Eszter Petra/0000-0002-0563-4876; Nagy, Péter/0000-0003-3393-235X; Pintér, Erika/0000-0001-9898-632X; Rakonczay, Zoltán/0000-0002-1499-3416}
}

@article{MTMT:34182063,
	title = {The effects of alcohol on anxiety-like, depression-like, and social behavior immediately and a day after binge drinking},
	url = {https://m2.mtmt.hu/api/publication/34182063},
	author = {Simon, Balázs and Thury, Attila Ágoston and Török, László and Földesi, Imre and Csabafi, Krisztina and Bagosi, Zsolt},
	doi = {10.1016/j.alcohol.2023.05.004},
	journal-iso = {ALCOHOL},
	journal = {ALCOHOL},
	volume = {112},
	unique-id = {34182063},
	issn = {0741-8329},
	year = {2023},
	eissn = {1873-6823},
	pages = {17-24},
	orcid-numbers = {Földesi, Imre/0000-0002-3329-8136; Csabafi, Krisztina/0000-0002-2008-7604}
}

@article{MTMT:34124825,
	title = {Inflammatory Orofacial Pain Activates Peptidergic Neurons and Upregulates the Oxytocin Receptor Expression in Trigeminal Ganglion},
	url = {https://m2.mtmt.hu/api/publication/34124825},
	author = {Kemenesi-Gedei, Péter Bátor and Csabafi, Krisztina and Karcsúné Kis, Gyöngyi},
	doi = {10.3390/biomedicines11092419},
	journal-iso = {BIOMEDICINES},
	journal = {BIOMEDICINES},
	volume = {11},
	unique-id = {34124825},
	abstract = {The majority of orofacial pain is caused by musculoskeletal and neuropathological diseases related to inflammatory processes that lead even to transcriptional alterations in the trigeminal ganglion (TG) neurons. The hypothalamic nonapeptide oxytocin has been reported to modulate nociception via binding and activating its receptor in primary sensory neurons. The purpose of this study was to analyze the gene expression of the oxytocin receptor (OTR), c-Fos, an indicator of neuronal activity, and α-calcitonin gene-related peptide (αCGRP), a characteristic neurotransmitter of the peptidergic trigeminal primary afferents in an animal model of inflammation-induced orofacial pain. Carrageenan was unilaterally injected into the vibrissal pads of male and female adult Wistar rats. RT-qPCR was performed to analyze the levels of mRNA expression in TGs 24 h after injection. The gene expression analysis revealed higher fold changes regarding the c-Fos (mean ± S.E: ♀: 3.9 ± 0.19; ♂: 3.55 ± 0.18) and αCGRP (♀: 2.84 ± 0.13; ♂: 3.39 ± 0.47) expression levels of mRNA, and a moderate rise in the expression of the OTR mRNA (♀: 1.52 ± 0.07; ♂: 1.49 ± 0.07) was observed in comparison to both vehicle(saline)-treated and untreated controls. Our results furnish evidence for inflammation-induced activation of peptidergic neurons, and it is suggested that oxytocin modulates inflammation-induced nociception by enhancing their signaling capacity due to its elevated expression in the sensory ganglion cells, thus providing new therapies for orofacial pain relief that target the OTRs.},
	year = {2023},
	eissn = {2227-9059},
	orcid-numbers = {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}
}

@mastersthesis{MTMT:34112876,
	title = {Improving the outcome of experimental acute pancreatitis: the effects of kynurenic acid, SZR-72 and analgesia [A kísérletes akut hasnyálmirigy-gyulladás kimenetelének javítása: a kinurénsav, az SZR-72 és a fájdalomcsillapítás hatása]},
	url = {https://m2.mtmt.hu/api/publication/34112876},
	author = {Kormányos, Eszter Sára},
	doi = {10.14232/phd.11543},
	publisher = {Universití of Szeged},
	unique-id = {34112876},
	year = {2023}
}