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 - 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 - Freiwan, Marah AU - Kovács, Mónika Gabriella AU - Kovács, Zsuzsanna AU - Szűcs, Gergő AU - Dinh, Hoa AU - Losonczi, Réka Hajnalka AU - Siska, Andrea AU - Kriston, András AU - Kovács, Ferenc AU - Horváth, Péter AU - Földesi, Imre AU - Cserni, Gábor AU - Dux, László AU - Csont, Tamás Bálint AU - Sárközy, Márta TI - Investigation of the Antiremodeling Effects of Losartan, Mirabegron and Their Combination on the Development of Doxorubicin-Induced Chronic Cardiotoxicity in a Rat Model JF - INTERNATIONAL JOURNAL OF MOLECULAR SCIENCES J2 - INT J MOL SCI VL - 23 PY - 2022 IS - 4 PG - 28 SN - 1661-6596 DO - 10.3390/ijms23042201 UR - https://m2.mtmt.hu/api/publication/32689754 ID - 32689754 N1 - Funding Agency and Grant Number: NKFIHNational Research, Development & Innovation Office (NRDIO) - Hungary [FK129094, GINOP-2.3.2-15-2016-00040]; Stipendium Hungaricum Program; Ministry of Human Capacities [TKP2021-EGA-32]; Ministry of Innovation and Technology of Hungary from the National Research, Development and Innovation Fund; Stipendium Hungaricum Scholarship; New National Excellence Program of the Ministry of Human Capacities [UNKP-21-3-SZTE-97, UNKP-21-3-SZTE-98, UNKP-20-5-SZTE-166]; Janos Bolyai Research Fellowship of the Hungarian Academy of SciencesHungarian Academy of Sciences; [EFOP-3.6.3VEKOP-16-2017-00009] Funding text: 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), Stipendium Hungaricum Program (to M.S. and L.D., funder: Tempus Public Foundation), and by the Ministry of Human Capacities TKP2021-EGA-32 (to T.C., Project no. TKP2021-EGA-32 has been implemented with the support provided by the Ministry of Innovation and Technology of Hungary from the National Research, Development and Innovation Fund, financed under the TKP2021-EGA funding scheme.) and by Stipendium Hungaricum Program (to M.S. and L.D., funder: Tempus Public Foundation). M.F. and D.H. were supported by the Stipendium Hungaricum Scholarship (funder: Tempus Public Foundation). M.G.K., Z.Z.A.K., and M.S. were supported by the New National Excellence Program of the Ministry of Human Capacities (UNKP-21-3-SZTE-97 to M.G.K., UNKP-21-3-SZTE-98 to Z.Z.A.K., and UNKP-20-5-SZTE-166 to M.S., funder: Ministry of Human Capacities). M.S. was 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-3.6.3VEKOP-16-2017-00009 project (funder: National Research, Development and Innovation Office). The APC was funded by Stipendium Hungaricum Program (funder: Tempus Public Foundation). AB - 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. LA - English DB - MTMT ER - TY - THES AU - Kovács, Zsuzsanna TI - 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] PB - Szegedi Tudományegyetem (SZTE) PY - 2021 SP - 48 DO - 10.14232/phd.11064 UR - https://m2.mtmt.hu/api/publication/32868192 ID - 32868192 LA - English DB - MTMT ER - TY - JOUR AU - Kovács, Mónika Gabriella AU - Kovács, Zsuzsanna AU - Varga, Zoltán AU - Szűcs, Gergő AU - Freiwan, Marah AU - Farkas, Katalin AU - Kővári, Bence AU - Cserni, Gábor AU - Kriston, András AU - Kovács, Ferenc AU - Horváth, Péter AU - Földesi, Imre AU - Csont, Tamás Bálint AU - Kahán, Zsuzsanna AU - Sárközy, Márta TI - Investigation of the Antihypertrophic and Antifibrotic Effects of Losartan in a Rat Model of Radiation-Induced Heart Disease JF - INTERNATIONAL JOURNAL OF MOLECULAR SCIENCES J2 - INT J MOL SCI VL - 22 PY - 2021 IS - 23 PG - 24 SN - 1661-6596 DO - 10.3390/ijms222312963 UR - https://m2.mtmt.hu/api/publication/32517976 ID - 32517976 N1 - MEDICS Research Group, Department of Biochemistry, Interdisciplinary Center of Excellence, Albert Szent-Györgyi Medical School, University of Szeged, Szeged, H-6720, Hungary Department of Oncotherapy, Albert Szent-Györgyi Medical School, University of Szeged, Szeged, H-6720, Hungary Department of Laboratory Medicine, Albert Szent-Györgyi Medical School, University of Szeged, Szeged, H-6720, Hungary Department of Pathology, Albert Szent-Györgyi Medical School, University of Szeged, Szeged, H-6720, Hungary Synthetic and Systems Biology Unit, Biological Research Centre, Eötvös Loránd Research Network, Szeged, H-6726, Hungary Single-Cell Technologies Ltd, Szeged, H-6726, Hungary Institute for Molecular Medicine Finland (FIMM), University of Helsinki, Helsinki, 00014, Finland Cited By :1 Export Date: 11 July 2022 Correspondence Address: Csont, T.; MEDICS Research Group, Hungary; email: csont.tamas@med.u-szeged.hu Correspondence Address: Sárközy, M.; MEDICS Research Group, Hungary; email: sarkozy.marta@med.u-szeged.hu 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 - Varga, Zoltán AU - Molnár-Gáspár, Renáta AU - Szűcs, Gergő AU - Kovács, Mónika Gabriella AU - Kovács, Zsuzsanna AU - Dux, László AU - Kahán, Zsuzsanna AU - Csont, Tamás Bálint TI - Pathomechanisms and therapeutic opportunities in radiation‑induced heart disease: from bench to bedside JF - CLINICAL RESEARCH IN CARDIOLOGY J2 - CLIN RES CARDIOL VL - 110 PY - 2021 IS - 4 SP - 507 EP - 531 PG - 25 SN - 1861-0684 DO - 10.1007/s00392-021-01809-y UR - https://m2.mtmt.hu/api/publication/31877554 ID - 31877554 N1 - MEDICS Research Group, Department of Biochemistry, Interdisciplinary Center of Excellence, University of Szeged, Szeged, 6720, Hungary Department of Oncotherapy, Faculty of Medicine, University of Szeged, Szeged, 6720, Hungary Department of Biochemistry, Faculty of Medicine, University of Szeged, Szeged, H-6720, Hungary Export Date: 28 May 2021 Correspondence Address: Sárközy, M.; MEDICS Research Group, Hungary; email: sarkozy.marta@med.u-szeged.hu Correspondence Address: Csont, T.; MEDICS Research Group, Hungary; email: csont.tamas@med.u-szeged.hu Correspondence Address: Kahán, Z.; Department of Oncotherapy, Hungary; email: kahan.zsuzsanna@med.u-szeged.hu Chemicals/CAS: alpha tocopherol, 1406-18-4, 1406-70-8, 52225-20-4, 58-95-7, 59-02-9; amifostine, 20537-88-6; atorvastatin, 134523-00-5, 134523-03-8; captopril, 62571-86-2; colchicine, 64-86-8; enalapril, 75847-73-3; fibroblast growth factor, 62031-54-3; fosinopril, 88889-14-9, 98048-97-6; gelatinase A, 146480-35-5; ibuprofen, 15687-27-1, 79261-49-7, 31121-93-4, 527688-20-6; intercellular adhesion molecule 1, 126547-89-5; interleukin 13, 148157-34-0; interleukin 8, 114308-91-7; interstitial collagenase, 9001-12-1; mevinolin, 75330-75-5; protein kinase B, 148640-14-6; Smad2 protein, 253862-89-4; Smad3 protein, 237417-78-6, 237417-96-8, 237418-00-7; trimetazidine, 13171-25-0, 5011-34-7 Funding details: Hungarian Scientific Research Fund, OTKA Funding details: Magyar Tudományos Akadémia, MTA, EFOP 3.6.3-VEKOP-16-2017-00009 Funding details: Emberi Eroforrások Minisztériuma, EMMI, 20391-3/2018/FEKUSTRAT, UNKP-19-3-SZTE-159, UNKP-19-3-SZTE-160, UNKP-19-4-I-SZTE-89, ÚNKP-20-4-SZTE-150, ÚNKP-20-5-SZTE-166 Funding details: Nemzeti Kutatási Fejlesztési és Innovációs Hivatal, NKFIH; hu:NKFI, EFOP-3.6.2-16-2017-00006, FK129094 Funding details: Wigner Fizikai Kutatóközpont, Magyar Tudományos Akadémia Funding details: Szegedi Tudományegyetem, SZTE Funding text 1: Open Access funding provided by University of Szeged. The work and publication were supported by the projects GINOP-2.3.2-15-2016-00040, NKFIH FK129094, EFOP-3.6.2-16-2017-00006 (LIVE LONGER) and by the Ministry of Human Capacities (20391-3/2018/FEKUSTRAT). MS, RG, MGK, and ZZAK were supported by the New National Excellence Program of the Ministry of Human Capacities (ÚNKP-20-5-SZTE-166, ÚNKP-20-4-SZTE-150, UNKP-19-4-I-SZTE-89, and UNKP-19-3-SZTE-159, UNKP-19-3-SZTE-160). MS is supported by the János Bolyai Research Fellowship of the Hungarian Academy of Sciences. MGK and ZZAK were supported by the EFOP 3.6.3-VEKOP-16-2017-00009. MEDICS Research Group, Department of Biochemistry, Interdisciplinary Center of Excellence, University of Szeged, Szeged, 6720, Hungary Department of Oncotherapy, Faculty of Medicine, University of Szeged, Szeged, 6720, Hungary Department of Biochemistry, Faculty of Medicine, University of Szeged, Szeged, H-6720, Hungary Export Date: 29 May 2021 Correspondence Address: Sárközy, M.; MEDICS Research Group, Hungary; email: sarkozy.marta@med.u-szeged.hu Correspondence Address: Csont, T.; MEDICS Research Group, Hungary; email: csont.tamas@med.u-szeged.hu Correspondence Address: Kahán, Z.; Department of Oncotherapy, Hungary; email: kahan.zsuzsanna@med.u-szeged.hu Chemicals/CAS: alpha tocopherol, 1406-18-4, 1406-70-8, 52225-20-4, 58-95-7, 59-02-9; amifostine, 20537-88-6; atorvastatin, 134523-00-5, 134523-03-8; captopril, 62571-86-2; colchicine, 64-86-8; enalapril, 75847-73-3; fibroblast growth factor, 62031-54-3; fosinopril, 88889-14-9, 98048-97-6; gelatinase A, 146480-35-5; ibuprofen, 15687-27-1, 79261-49-7, 31121-93-4, 527688-20-6; intercellular adhesion molecule 1, 126547-89-5; interleukin 13, 148157-34-0; interleukin 8, 114308-91-7; interstitial collagenase, 9001-12-1; mevinolin, 75330-75-5; protein kinase B, 148640-14-6; Smad2 protein, 253862-89-4; Smad3 protein, 237417-78-6, 237417-96-8, 237418-00-7; trimetazidine, 13171-25-0, 5011-34-7 Funding details: Hungarian Scientific Research Fund, OTKA Funding details: Magyar Tudományos Akadémia, MTA, EFOP 3.6.3-VEKOP-16-2017-00009 Funding details: Emberi Eroforrások Minisztériuma, EMMI, 20391-3/2018/FEKUSTRAT, UNKP-19-3-SZTE-159, UNKP-19-3-SZTE-160, UNKP-19-4-I-SZTE-89, ÚNKP-20-4-SZTE-150, ÚNKP-20-5-SZTE-166 Funding details: Nemzeti Kutatási Fejlesztési és Innovációs Hivatal, NKFIH; hu:NKFI, EFOP-3.6.2-16-2017-00006, FK129094 Funding details: Wigner Fizikai Kutatóközpont, Magyar Tudományos Akadémia Funding details: Szegedi Tudományegyetem, SZTE Funding text 1: Open Access funding provided by University of Szeged. The work and publication were supported by the projects GINOP-2.3.2-15-2016-00040, NKFIH FK129094, EFOP-3.6.2-16-2017-00006 (LIVE LONGER) and by the Ministry of Human Capacities (20391-3/2018/FEKUSTRAT). MS, RG, MGK, and ZZAK were supported by the New National Excellence Program of the Ministry of Human Capacities (ÚNKP-20-5-SZTE-166, ÚNKP-20-4-SZTE-150, UNKP-19-4-I-SZTE-89, and UNKP-19-3-SZTE-159, UNKP-19-3-SZTE-160). MS is supported by the János Bolyai Research Fellowship of the Hungarian Academy of Sciences. MGK and ZZAK were supported by the EFOP 3.6.3-VEKOP-16-2017-00009. LA - English DB - MTMT ER -