TY - JOUR AU - Dinh, Hoa AU - Kovács, Zsuzsanna AU - Kis, Merse AU - Kupecz, Klaudia AU - Sejben, Anita AU - Szűcs, Gergő AU - Márványkövi, Fanni AU - Siska, Andrea AU - Freiwan, Marah AU - Pósa, Szonja Polett AU - Galla, Zsolt AU - Ibos, Katalin Eszter AU - Bodnár, Éva AU - Lauber, Gülsüm Yilmaz AU - Goncalves, Ana Isabel Antunes AU - Acar, Eylem AU - Kriston, András AU - Kovács, Ferenc AU - Horváth, Péter AU - Bozsó, Zsolt AU - Tóth, Gábor AU - Földesi, Imre AU - Monostori, Péter AU - Cserni, Gábor AU - Podesser, Bruno K. AU - Lehoczki, Andrea Marianna AU - Pokreisz, Peter AU - Kiss, Attila AU - Dux, László AU - Csabafi, Krisztina AU - Sárközy, Márta TI - Role of the kisspeptin-KISS1R axis in the pathogenesis of chronic kidney disease and uremic cardiomyopathy JF - GEROSCIENCE: OFFICIAL JOURNAL OF THE AMERICAN AGING ASSOCIATION (AGE) J2 - GEROSCIENCE VL - 46 PY - 2024 IS - 2 SP - 2463 EP - 2488 PG - 26 SN - 2509-2715 DO - 10.1007/s11357-023-01017-8 UR - https://m2.mtmt.hu/api/publication/34395398 ID - 34395398 N1 - Department of Biochemistry and Interdisciplinary Centre of Excellence, Albert Szent-Györgyi Medical School, University of Szeged, Szeged, 6720, Hungary Department of Biochemistry, Bach Mai Hospital, Hanoi, 100000, Viet Nam Department of Pathophysiology, Albert Szent-Györgyi Medical School, University of Szeged, Szeged, 6720, Hungary Department of Pathology, Albert Szent-Györgyi Medical School, University of Szeged, Szeged, 6720, Hungary Department of Laboratory Medicine, Albert Szent-Györgyi Medical School, University of Szeged, Szeged, 6720, Hungary Metabolic and Newborn Screening Laboratory, Department of Pediatrics, Albert Szent-Györgyi Medical School, University of Szeged, Szeged, 6720, Hungary Ludwig Boltzmann Institute for Cardiovascular Research at Center for Biomedical Research and Translational Surgery, Medical University of Vienna, Vienna, 1090, Austria Synthetic and Systems Biology Unit, Biological Research Centre, Eötvös Loránd Research Network, Szeged, 6726, Hungary Single-Cell Technologies Ltd, Szeged, 6726, Hungary Institute for Molecular Medicine Finland (FIMM), University of Helsinki, Helsinki, 00014, Finland Department of Medical Chemistry, Albert Szent-Györgyi Medical School, University of Szeged, Szeged, 6720, Hungary Departments of Hematology and Stem Cell Transplantation, South Pest Central Hospital, National Institute of Hematology and Infectious Diseases, Saint Ladislaus Campus, Budapest, Hungary Export Date: 16 April 2024 Correspondence Address: Dux, L.; Department of Biochemistry and Interdisciplinary Centre of Excellence, Hungary; email: dux.laszlo@med.u-szeged.hu Correspondence Address: Sárközy, M.; Department of Biochemistry and Interdisciplinary Centre of Excellence, Hungary; email: martasarkozy@gmail.com AB - 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. LA - English DB - MTMT ER - TY - JOUR AU - Ibos, Katalin Eszter AU - Bodnár, Éva AU - Dinh, Hoa AU - Kis, Merse AU - Márványkövi, Fanni AU - Kovács, Zsuzsanna AU - Siska, Andrea AU - Földesi, Imre AU - Galla, Zsolt AU - Monostori, Péter AU - Szatmári, István AU - Simon, Péter AU - Sárközy, Márta AU - Csabafi, Krisztina TI - Chronic kidney disease may evoke anxiety by altering CRH expression in the amygdala and tryptophan metabolism in rats JF - PFLUGERS ARCHIV-EUROPEAN JOURNAL OF PHYSIOLOGY J2 - PFLUG ARCH EUR J PHY VL - 476 PY - 2024 IS - 2 SP - 179 EP - 196 PG - 18 SN - 0031-6768 DO - 10.1007/s00424-023-02884-y UR - https://m2.mtmt.hu/api/publication/34394136 ID - 34394136 AB - 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. LA - English DB - MTMT ER - TY - THES AU - Márványkövi, Fanni TI - 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] PB - Szegedi Tudományegyetem PY - 2023 SP - 57 DO - 10.14232/phd.11611 UR - https://m2.mtmt.hu/api/publication/34126375 ID - 34126375 AB - 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. LA - English DB - MTMT ER - TY - JOUR AU - Dinh, Hoa AU - Kovács, Zsuzsanna AU - Márványkövi, Fanni AU - Kis, Merse AU - Kupecz, Klaudia AU - Szűcs, Gergő AU - Freiwan, Marah AU - Lauber, Gülsüm Yilmaz AU - Acar, Eylem AU - Siska, Andrea AU - Ibos, Katalin Eszter AU - Bodnár, Éva AU - Kriston, András AU - Kovács, Ferenc AU - Horváth, Péter AU - Földesi, Imre AU - Cserni, Gábor AU - Podesser, Bruno K. AU - Pokreisz, Peter AU - Kiss, Attila AU - Dux, László AU - Csabafi, Krisztina AU - Sárközy, Márta TI - The kisspeptin-1 receptor antagonist peptide-234 aggravates uremic cardiomyopathy in a rat model JF - SCIENTIFIC REPORTS J2 - SCI REP VL - 13 PY - 2023 IS - 1 PG - 16 SN - 2045-2322 DO - 10.1038/s41598-023-41037-0 UR - https://m2.mtmt.hu/api/publication/34123594 ID - 34123594 N1 - Department of Biochemistry and Interdisciplinary Centre of Excellence, Albert Szent-Györgyi Medical School, University of Szeged, Szeged, 6720, Hungary Department of Biochemistry, Bach Mai Hospital, Hanoi, 100000, Viet Nam Ludwig Boltzmann Institute for Cardiovascular Research at Center for Biomedical Research and Translational Surgery, Medical University of Vienna, Vienna, A1090, Austria Department of Laboratory Medicine, Albert Szent-Györgyi Medical School, University of Szeged, Szeged, 6720, Hungary Department of Pathophysiology, Albert Szent-Györgyi Medical School, University of Szeged, Szeged, 6720, Hungary Synthetic and Systems Biology Unit, Biological Research Centre, Eötvös Loránd Research Network, Szeged, 6726, Hungary Single-Cell Technologies Ltd, Szeged, 6726, Hungary Institute for Molecular Medicine Finland (FIMM), University of Helsinki, Helsinki, 00014, Finland Department of Pathology, Albert Szent-Györgyi Medical School, University of Szeged, Szeged, 6720, Hungary Export Date: 7 September 2023 Correspondence Address: Dux, L.; Department of Biochemistry and Interdisciplinary Centre of Excellence, Hungary; email: dux.laszlo@med.u-szeged.hu Correspondence Address: Sárközy, M.; Department of Biochemistry and Interdisciplinary Centre of Excellence, Hungary; email: sarkozy.marta@med.u-szeged.hu Funding details: BO/00532/23/5, UNKP-19-3-SZTE-160, UNKP-20-5-SZTE-166 Funding details: TSZ:34232-3/2016/INTFIN Funding details: 6177 Funding details: Magyar Tudományos Akadémia, MTA Funding details: Nemzeti Kutatási Fejlesztési és Innovációs Hivatal, NKFIH, EFOP-3.6.2-16-2017-00006, GINOP-2.3.2-15-2016-00040 Funding details: Tempus Közalapítvány, TPF Funding details: Szegedi Tudományegyetem, SZTE Funding text 1: Open access funding provided by University of Szeged. This research was funded by the projects NKFIH FK129094 (to M.S., funder: National Research, Development and Innovation Office), GINOP-2.3.2-15-2016-00040 (to L.D., funder: National Research, Development and Innovation Office), EFOP-3.6.2-16-2017-00006 (to K.C., funder: National Research, Development and Innovation Office), Stipendium Hungaricum Program (to M.S. and L.D., funder: Tempus Public Foundation), and Ludwig Boltzmann Institute for Cardiovascular Research, Vienna, Austria. D.H. and M.F. were supported by the Stipendium Hungaricum Scholarship (funder: Tempus Public Foundation). H. D. was supported by the Albert Szent-Györgyi Scholarship for Ph.D. students (funder: University of Szeged, Albert Szent-Györgyi Medical School, Szeged, Hungary) and Bach Mai Hospital, Hanoi, Vietnam. M.S. and Z.Z.A.K. were supported by the New National Excellence Program of the Ministry of Human Capacities, Hungary (UNKP-20-5-SZTE-166 and UNKP-19-3-SZTE-160). M.S. was supported by the János Bolyai Research Scholarship (BO/00532/23/5) of the Hungarian Academy of Sciences. Z.Z.A.K. was supported by the EFOP 3.6.3-VEKOP-16-2017-00009 (funder: National Research, Development and Innovation Office). A.K. was supported by Theodor Körner Founds, Austria. F.M. was supported by the Szeged Scientists Academy Program (TSZ:34232-3/2016/INTFIN, Hungary). The publication was supported by the University of Szeged Open Access Found (6177). AB - 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. LA - English DB - MTMT ER - TY - JOUR AU - Sárközy, Márta AU - Watzinger, Simon AU - Kovács, Zsuzsanna AU - Acar, Eylem AU - Márványkövi, Fanni AU - Szűcs, Gergő AU - Lauber, Gülsüm Yilmaz AU - Galla, Zsolt AU - Siska, Andrea AU - Földesi, Imre AU - Fintha, Attila AU - Kriston, András AU - Kovács, Ferenc AU - Horváth, Péter AU - Kővári, Bence AU - Cserni, Gábor AU - Krenács, Tibor AU - Szabó, Petra Lujza AU - Szabó, Gábor Tamás AU - Monostori, Péter AU - Zins, Karin AU - Abraham, Dietmar AU - Csont, Tamás Bálint AU - Pokreisz, Peter AU - Podesser, Bruno K. AU - Kiss, Attila TI - Neuregulin-1β Improves Uremic Cardiomyopathy and Renal Dysfunction in Rats JF - JACC:BASIC TO TRANSLATIONAL SCIENCE J2 - JACC-BASIC TRANSL SC VL - 8 PY - 2023 IS - 9 SP - 1160 EP - 1176 PG - 17 SN - 2452-302X DO - 10.1016/j.jacbts.2023.03.003 UR - https://m2.mtmt.hu/api/publication/33941648 ID - 33941648 LA - English DB - MTMT ER - TY - JOUR AU - Sárközy, Márta AU - Márványkövi, Fanni AU - Szűcs, Gergő AU - Kovács, Zsuzsanna AU - Szabó, Márton Richárd AU - Molnár-Gáspár, Renáta AU - Siska, Andrea AU - Kővári, Bence AU - Cserni, Gábor AU - Földesi, Imre AU - Csont, Tamás Bálint TI - Ischemic preconditioning protects the heart against ischemia-reperfusion injury in chronic kidney disease in both males and females JF - BIOLOGY OF SEX DIFFERENCES J2 - BIOL SEX DIFFER VL - 12 PY - 2021 IS - 1 PG - 20 SN - 2042-6410 DO - 10.1186/s13293-021-00392-1 UR - https://m2.mtmt.hu/api/publication/32191180 ID - 32191180 N1 - Funding Agency and Grant Number: Ministry of Human Capacities [20391-3/2018/FEKUSTRAT, TSZ:34232-3/2016/INTFIN]; New National Excellence Program of the Ministry of Human Capacities [UNKP-20-5-SZTE-166, UNKP-19-4-SZTE-89, UNKP-19-2-SZTE-77, UNKP-20-4-SZTE-150, UNKP19-3-SZTE-269]; Janos Bolyai Research Fellowship of the Hungarian Academy of SciencesHungarian Academy of Sciences; Szeged Scientists Academy Program; [GINOP-2.3.2-152016-00040]; [NKFIH K115990]; [NKFIH FK129094]; [EFOP-3.6.2-16-2017-00006] Funding text: The work and publication were supported by the projects GINOP-2.3.2-152016-00040, NKFIH K115990, NKFIH FK129094, EFOP-3.6.2-16-2017-00006 (LIVE LONGER), and by the Ministry of Human Capacities (20391-3/2018/FEKUSTRAT). MS, FMM, RG, and MRS were supported by the New National Excellence Program of the Ministry of Human Capacities (UNKP-20-5-SZTE-166, UNKP-19-4-SZTE-89, UNKP-19-2-SZTE-77, UNKP-20-4-SZTE-150 and UNKP19-3-SZTE-269). MS is supported by the Janos Bolyai Research Fellowship of the Hungarian Academy of Sciences. FMM was supported by the Szeged Scientists Academy Program. The Szeged Scientists Academy Program of the Foundation for the Future of Biomedical Sciences in Szeged is implemented with the support of the Ministry of Human Capacities (TSZ:34232-3/2016/INTFIN). LA - English DB - MTMT ER - TY - JOUR AU - Kovács, Zsuzsanna AU - Szűcs, Gergő AU - Freiwan, Marah AU - Kovács, Mónika Gabriella AU - Márványkövi, Fanni AU - Dinh, Hoa AU - Siska, Andrea AU - Farkas, Katalin AU - Kovács, Ferenc AU - Kriston, András AU - Horváth, Péter AU - Kővári, Bence AU - Cserni, Bálint Gábor AU - Cserni, Gábor AU - Földesi, Imre AU - Csont, Tamás Bálint AU - Sárközy, Márta TI - Comparison of the antiremodeling effects of losartan and mirabegron in a rat model of uremic cardiomyopathy JF - SCIENTIFIC REPORTS J2 - SCI REP VL - 11 PY - 2021 IS - 1 PG - 18 SN - 2045-2322 DO - 10.1038/s41598-021-96815-5 UR - https://m2.mtmt.hu/api/publication/32172362 ID - 32172362 N1 - Funding Agency and Grant Number: NKFIHNational Research, Development & Innovation Office (NRDIO) - Hungary [FK129094, K115990, EFOP-3.6.2-16-2017-00006]; Ministry of Human Capacities [20391-3/2018/FEKUSTRAT]; New National Excellence Program of the Ministry of Human Capacities [UNKP-20-5-SZTE-166, UNKP-19-4SZTE-89, UNKP-19-3-SZTE-160, UNKP-19-3-SZTE-159, UNKP-19-2-SZTE-77]; Janos Bolyai Research Fellowship of the Hungarian Academy of SciencesHungarian Academy of Sciences; Szeged Scientists Academy Program; Ministry of Human Resources [TSZ:34232-3/2016/INTFIN]; [GINOP-2.3.2-15-2016 00040]; [EFOP-3.6.3-VEKOP-16-2017-00009] Funding text: The work and publication were supported by the projects GINOP-2.3.2-15-2016 00040, by the NKFIH FK129094 (to M.S.), NKFIH K115990 (to T.C), EFOP-3.6.2-16-2017-00006 (LIVE LONGER), and by the Ministry of Human Capacities (20391-3/2018/FEKUSTRAT). M.S., Z.Z.A.K., M.G.K., and F.M.M., were supported by the New National Excellence Program of the Ministry of Human Capacities (UNKP-20-5-SZTE-166, UNKP-19-4SZTE-89, UNKP-19-3-SZTE-160, UNKP-19-3-SZTE-159, and UNKP-19-2-SZTE-77). M.S. is supported by the Janos Bolyai Research Fellowship of the Hungarian Academy of Sciences. Z.Z.A.K. and M.G.K. were supported by the EFOP-3.6.3-VEKOP-16-2017-00009 project. FM was supported by the Szeged Scientists Academy Program. The Szeged Scientists Academy Program of the Foundation for the Future of Biomedical Sciences in Szeged is implemented with the support of the Ministry of Human Resources (TSZ:34232-3/2016/INTFIN). LA - English DB - MTMT ER - TY - JOUR AU - Sárközy, Márta AU - Márványkövi, Fanni AU - Szűcs, Gergő AU - Molnár-Gáspár, Renáta AU - Dajka, Dalma AU - Siska, Andrea AU - Földesi, Imre AU - Csont, Tamás Bálint TI - A nemi különbségek hatása a szív iszkémiás prekondícionálhatóságára krónikus veseelégtelenségben [The effect of gender differences on cardiac ischemic preconditioning in chronic kidney disease] JF - CARDIOLOGIA HUNGARICA J2 - CARDIOL HUNG VL - 49 PY - 2019 IS - Supplementum B SP - B32 EP - B33 PG - 2 SN - 0133-5596 UR - https://m2.mtmt.hu/api/publication/31289428 ID - 31289428 N1 - Támogatások: Modern orvostudományi diagnosztikus eljárások és terápiák fejlesztése transzlációs megközelítésbe...(EFOP-3.6.2-16-2017-00006) Támogató: EFOP GINOP-2.3.2-15-2016-00040 (MyoTeam) NKFI_FK_129094 NKFIH K115990 Bolyai János Kutatási Ösztöndíj UNKP-18-4-I-SZTE-63 Szegedi Tudós Akadémia program (EMMI, TSZ:34232-3/2016/INTFIN LA - English DB - MTMT ER - TY - CHAP AU - Sárközy, Márta AU - Molnár-Gáspár, Renáta AU - Zvara, Ágnes AU - Siska, Andrea AU - Kővári, Bence AU - Szűcs, Gergő AU - Márványkövi, Fanni AU - Kovács, Mónika Gabriella AU - Diószegi, Petra AU - Bodai, László AU - Zsindely, Nóra AU - Pipicz, Márton AU - Gömöri, Kamilla AU - Kiss, Krisztina AU - Bencsik, Péter AU - Cserni, Gábor AU - Puskás, László AU - Földesi, Imre AU - Thum, Thomas AU - Bátkai, Sándor AU - Csont, Tamás Bálint ED - Bagdy, György TI - Krónikus veseelégtelenségben megemelkedik a prohipertrófiás miR-212 bal kamrai expressziója T2 - FAMÉ 2019 Magyar Kísérletes és Klinikai Farmakológiai Társaság; Magyar Anatómus Társaság; Magyar Mikrocirkulációs és Vaszkuláris Biológiai Társaság; Magyar Élettani Társaság PB - Expert-Quality Kongresszusi és Utazási Iroda CY - Budapest SN - 9786158129909 PY - 2019 SP - 107 EP - 108 PG - 2 UR - https://m2.mtmt.hu/api/publication/31289422 ID - 31289422 N1 - Új Nemzeti Kiválóság Program (UNKP-17-2-I-SZTE-9, UNKP-17-4-I-SZTE-43, UNKP-18-4-63) NKFIH K115990,GINOP-2.3.2-15-2016-00040, Szegedi Tudós Akadémia program (EMMI, TSZ:34232-3/2016/INTFIN) LA - Hungarian DB - MTMT ER - TY - GEN AU - Sárközy, Márta AU - Molnár-Gáspár, Renáta AU - Zvara, Ágnes AU - Siska, Andrea AU - Kővári, Bence AU - Szűcs, Gergő AU - Márványkövi, Fanni AU - Kovács, Mónika Gabriella AU - Diószegi, Petra AU - Bodai, László AU - Zsindely, Nóra AU - Pipicz, Márton AU - Gömöri, Kamilla AU - Kiss, Krisztina AU - Bencsik, Péter AU - Cserni, Gábor AU - Puskás, L ászló AU - Földesi, Imre AU - Thum, Thomas AU - Bátkai, Sándor AU - Csont, Tamás Bálint TI - Chronic kidney disease induces left ventricular overexpression of the pro-hypertrophic microRNA-212 PY - 2019 UR - https://m2.mtmt.hu/api/publication/31289397 ID - 31289397 N1 - Our project was by the projects GINOP-2.3.2-15-2016-00006, NKFIH K115990, NKFIH FK129094, 20391-3/2018/FEKUSTRAT, UNKP-18-4-SZTE-63, M. Sarkozy was supported by the János Bolyai Research Scholarship of the Hungarian Academy of Sciences. LA - English DB - MTMT ER -