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 - 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 - Sztretye, Mónika AU - Singlár, Zoltán AU - Ganbat, Nyamkhuu AU - Al-Gaadi, Dána AU - Szabó, Kitti AU - Köhler, Zoltán Márton AU - Dux, László AU - Keller-Pintér, Anikó AU - Csernoch, László AU - Szentesi, Péter TI - Unravelling the Effects of Syndecan-4 Knockdown on Skeletal Muscle Functions JF - INTERNATIONAL JOURNAL OF MOLECULAR SCIENCES J2 - INT J MOL SCI VL - 24 PY - 2023 IS - 8 PG - 19 SN - 1661-6596 DO - 10.3390/ijms24086933 UR - https://m2.mtmt.hu/api/publication/33742741 ID - 33742741 AB - The remodelling of the extracellular matrix plays an important role in skeletal muscle development and regeneration. Syndecan-4 is a cell surface proteoglycan crucial for muscle differentiation. Syndecan-4−/− mice have been reported to be unable to regenerate following muscle damage. To investigate the consequences of the decreased expression of Syndecan-4, we have studied the in vivo and in vitro muscle performance and the excitation–contraction coupling machinery in young and aged Syndecan-4+/− (SDC4) mice. In vivo grip force was decreased significantly as well as the average and maximal speed of voluntary running in SDC4 mice, regardless of their age. The maximal in vitro twitch force was reduced in both EDL and soleus muscles from young and aged SDC4 mice. Ca2+ release from the sarcoplasmic reticulum decreased significantly in the FDB fibres of young SDC4 mice, while its voltage dependence was unchanged regardless of age. These findings were present in muscles from young and aged mice as well. On C2C12 murine skeletal muscle cells, we have also found altered calcium homeostasis upon Syndecan-4 silencing. The decreased expression of Syndecan-4 leads to reduced skeletal muscle performance in mice and altered motility in C2C12 myoblasts via altered calcium homeostasis. The altered muscle force performance develops at an early age and is maintained throughout the life course of the animal until old age. LA - English DB - MTMT ER - TY - JOUR AU - Köhler, Zoltán Márton AU - Trencsényi, György AU - Juhász, László AU - Zvara, Ágnes AU - Szabó, P Judit AU - Dux, László AU - Puskás, László AU - Rovó, László AU - Keller-Pintér, Anikó TI - Tilorone increases glucose uptake in vivo and in skeletal muscle cells by enhancing Akt2/AS160 signaling and glucose transporter levels JF - JOURNAL OF CELLULAR PHYSIOLOGY J2 - J CELL PHYSIOL VL - 238 PY - 2023 IS - 5 SP - 1080 EP - 1094 PG - 15 SN - 0021-9541 DO - 10.1002/jcp.30998 UR - https://m2.mtmt.hu/api/publication/33683749 ID - 33683749 N1 - Funding Agency and Grant Number: National Research, Development and Innovation Office of Hungary; National Research, Development and Innovation Fund; Janos Bolyai Research Scholarship of the Hungarian Academy of Sciences; New National Excellence Program of the Ministry for Innovation and Technology Sciences; University of Szeged Open Access Fund Funding text: National Research, Development and Innovation Office of Hungary; National Research, Development and Innovation Fund;Janos Bolyai Research Scholarship of the Hungarian Academy of Sciences; New National Excellence Program of the Ministry for Innovation and Technology Sciences;University of Szeged Open Access Fund LA - English DB - MTMT ER - TY - GEN ED - Dux, László ED - Bruno, Podesser TI - Special Issue" Pharmacology of Antioxidants" PY - 2022 UR - https://m2.mtmt.hu/api/publication/33713899 ID - 33713899 AB - Oxidation and reduction, basically the release and uptake of electrons, are essential phenomena in life. Our molecular systems, cellular and subcellular components are more prone to be damaged by unwanted oxidation than by reduction due to our oxidative atmosphere. This oxidative damage is even more aggravated by the generation of Reactive Oxygen and Nitrogen Species and /or by Free Oxygen Radicals. Natural and synthetic Antioxidants are known to be useful in preventing and alleviating these damages in almost all areas of medical sciences. Although generally considered advantageous, in some molecular systems, the proper functionality requires the oxidised state of certain substances, making antioxidants unnecessary, even harmful under certain conditions. A deeper understanding of the pharmacology, the molecular mechanism of natural and synthetic antioxidants may promote and help the effective application thereof in particular areas of cardiovascular diseases, during exercise and aging in skeletal and heart muscles, as well as in neurological disorders, diabetes mellitus, and cancerous processes. The present issue aims to collect and document new findings in the pharmacology of natural and synthetic antioxidants, old and new, to promote and support their application in the most important areas of recent day’s human medicine. LA - English DB - MTMT ER - TY - CONF AU - Fazekas, Szuzina AU - Becsky, Dániel AU - Horváth, Péter AU - Deák, Ágota AU - Janovák, László AU - Dux, László AU - Keller-Pintér, Anikó TI - AZ EXOSZÓMÁK BEFOLYÁSOLJÁK A SDC4-FÜGGŐ SEJTMOZGÁST T2 - 51. Membrán-Transzport Konferencia PY - 2022 SP - 20 UR - https://m2.mtmt.hu/api/publication/32908656 ID - 32908656 LA - Hungarian DB - MTMT ER - TY - CONF AU - Köhler, Zoltán Márton AU - Trencsényi, György AU - Juhász, László AU - Zvara, Ágnes AU - Szabó, Judit AU - Dux, László AU - Puskás, László AU - Rovó, László AU - Keller-Pintér, Anikó TI - A tiloron javítja a glükózfelvételt in vivo és in vitro vázizomsejtekben a BMP jelátvitel és glükóz transzporter szintek növelésével T2 - 51. Membrán-Transzport Konferencia PY - 2022 PG - 1 UR - https://m2.mtmt.hu/api/publication/32908634 ID - 32908634 LA - Hungarian DB - MTMT ER - TY - CONF AU - Tóth, Enikő AU - Szabó, Kitti AU - Vég, Attila Gergely AU - Becsky, Dániel AU - Dux, László AU - Rovó, László AU - Keller-Pintér, Anikó TI - A BMP-INDUKTOR TILORON ANTIFIBROTIKUS HATÁSÁNAK VIZSGÁLATA LÉGÚTI FIBROBLASZTOKBAN T2 - 51. Membrán-Transzport Konferencia PY - 2022 SP - 82 UR - https://m2.mtmt.hu/api/publication/32908632 ID - 32908632 LA - Hungarian DB - MTMT ER - TY - CONF AU - Dukay, Brigitta AU - Bódai, Zsófia AU - Csefová, Alexandra AU - Hajdu, Petra AU - Ruppert, Zsófia AU - Penke, Botond AU - Fülöp, Lívia AU - Szabó, Kitti AU - Keller-Pintér, Anikó AU - Dux, László AU - Gombos, Imre AU - Török, Zsolt AU - Sántha, Miklós AU - Tóth, E. Melinda TI - A rendszeres testmozgás izom- és agyszövetre kifejtett nem-függő hatásainak vizsgálata a hiperlipidémia egérmodelljében T2 - 51. Membrán-Transzport Konferencia PY - 2022 PG - 1 UR - https://m2.mtmt.hu/api/publication/32908630 ID - 32908630 LA - Hungarian DB - MTMT ER - TY - CONF AU - Köhler, Zoltán Márton AU - Trencsényi, György AU - Horváth, Barnabás AU - Halász, Judit AU - Szenci-Kaszás, Balázs AU - Szabó, Kitti AU - Kovács, Mercédesz AU - Dux, László AU - Schaff, Zsuzsa AU - Rovó, László AU - Keller-Pintér, Anikó TI - A tiloron metabolikus hatásai magas zsírtartalmú diéta esetén in vivo egérmodellben T2 - 51. Membrán-Transzport Konferencia PY - 2022 SP - 43 EP - 43 PG - 1 UR - https://m2.mtmt.hu/api/publication/32908627 ID - 32908627 LA - Hungarian DB - MTMT ER -