TY - JOUR AU - Zádor, Ernő TI - Characterization of Skeletal Muscle Regeneration Revealed a Novel Growth Network Induced by Molecular Acupuncture-like Transfection JF - BIOMOLECULES J2 - BIOMOLECULES VL - 14 PY - 2024 IS - 3 PG - 14 SN - 2218-273X DO - 10.3390/biom14030363 UR - https://m2.mtmt.hu/api/publication/34757257 ID - 34757257 AB - The low efficiency of in vivo transfection of a few fibres revealed a novel tissue network that temporally amplified growth stimulation in the entire regenerating rat soleus muscle. This acupuncture-like effect was demonstrated when the fibres began to grow after complete fibre degradation, synchronous inflammation, myoblast and myotube formation. Neonatal sarcoplasmic/endoplasmic reticulum ATPase (SERCA1b) was first detected in this system. The neonatal, fast and slow SERCA isoforms displayed consequent changes with innervation and differentiation, recapitulating events in muscle development. In vivo transfection of myotubes with plasmids expressing dominant negative Ras or a calcineurin inhibitor peptide (Cain/cabin) proved that expression of the slow myosin heavy chain and the slow muscle type SERCA2a are differentially regulated. In vivo transfection of a few nuclei of myotubes with dnRas or SERCA1b shRNA stimulated fibre size growth in the whole regenerating muscle but only until the full size had been reached. Growth stimulation by Ras and SERCA1b antisense was abolished by co-transfection of Cain or with perimuscular injection of IL4 antibody. This revealed a novel signalling network resembling scale-free networks which, starting from transfected fibre myonuclei as “hubs”, can amplify growth stimulation uniformly in the entire regenerating muscle. LA - English DB - MTMT ER - TY - JOUR AU - Zádor, Ernő TI - Paradoxical Effect of Caloric Restriction on Overload-Induced Muscle Growth in Diastolic Heart Failure JF - JACC:BASIC TO TRANSLATIONAL SCIENCE J2 - JACC-BASIC TRANSL SC VL - 9 PY - 2024 IS - 2 SP - 241 EP - 243 PG - 3 SN - 2452-302X DO - 10.1016/j.jacbts.2023.11.011 UR - https://m2.mtmt.hu/api/publication/34754547 ID - 34754547 LA - English DB - MTMT ER - 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 - Keller-Pintér, Anikó AU - Korcsmáros, Tamás AU - Vellai, Tibor TI - Managing type 2 diabetes: targeting a microbial enzyme as a novel treatment option JF - SIGNAL TRANSDUCTION AND TARGETED THERAPY J2 - SIGNAL TRANSDUCT TAR VL - 8 PY - 2023 IS - 1 PG - 3 SN - 2095-9907 DO - 10.1038/s41392-023-01694-z UR - https://m2.mtmt.hu/api/publication/34435797 ID - 34435797 N1 - Besorolása összefoglaló cikk a központi MTMT adminisztrátorokkal történt egyeztetés és az MTA V. Osztályának képviselője által végzett tartalmi vizsgálat alapján. (BCS, SZTE admin4, 2024-03-13) LA - English DB - MTMT ER - TY - JOUR AU - Nógrádi-Halmi, Dóra AU - Erdélyi-Furka, Barbara Fanni AU - Molnár-Gáspár, Renáta AU - Csont, Tamás Bálint TI - Triptofán-származékok, mint lehetséges biomarkerek és terápiás célpontok egyes kardiovaszkuláris megbetegedésekben [Tryptophan metabolites as potential biomarkers and therapeutic targets in certain cardiovascular diseases] JF - CARDIOLOGIA HUNGARICA J2 - CARDIOL HUNG VL - 53 PY - 2023 IS - 5 SP - 468 EP - 475 PG - 8 SN - 0133-5596 DO - 10.26430/CHUNGARICA.2023.53.5.468 UR - https://m2.mtmt.hu/api/publication/34416566 ID - 34416566 AB - A gyulladásos folyamatok kiemelkedő szereppel bírnak a vezető halálokok közé sorolható koszorúér-betegségek patomechanizmusában és progressziójában. Ismert, hogy az ezen folyamatok során felszabaduló proinflammatorikus molekulák képesek elősegíteni a triptofán-aminosav kinurenin-útvonalon történő lebomlását. Ez számos immunmodulátor kinurenin-metabolit felszabadulását teszi lehetővé, amelyek között egyaránt szerepelnek jótékony, valamint káros hatással bíró vegyületek. Mai tudásunk szerint a különböző kinurenin-származékok előállításáért felelős metabolikus útvonalak egyensúlyának felborulása fontos szereppel bírhat bizonyos betegségek, köztük egyes kardiovaszkuláris megbetegedések kórlefolyásában. Több tanulmány is alátámasztja, hogy számos kinurenin-metabolit koncentrációjának változása kimutatható koszorúér-betegségben szenvedő páciensektől nyert vér- és/vagy vizeletmintákban. Egyes közlemények szerint bizonyos kinureninek szérumszintje korrelálhat a koronáriabetegségek progressziójával. Összefoglaló tanulmányunk célja annak áttekintése, hogy a kinureninek szereppel bírhatnak-e a jövőben egyes kardiovaszkuláris betegségek rizikóbecslésében, mint biomarkerek, illetve segíthetik-e új terápiás stratégiák kidolgozását. LA - Hungarian DB - MTMT ER - TY - JOUR AU - Pipicz, Márton AU - Demján, Virág AU - Csonka, Csaba AU - Csont, Tamás Bálint TI - Piroptózis, PANoptózis és ferroptózis a szív iszkémia/reperfúziós károsodásában JF - CARDIOLOGIA HUNGARICA J2 - CARDIOL HUNG VL - 53 PY - 2023 IS - 5 SP - 451 EP - 458 PG - 8 SN - 0133-5596 DO - 10.26430/CHUNGARICA.2023.53.5.451 UR - https://m2.mtmt.hu/api/publication/34416562 ID - 34416562 AB - Az intenzív kutatások ellenére továbbra sem rendelkezünk olyan kardioprotektív gyógyszerekkel, amelyek a szív iszkémia/reperfúziós (I/R) károsodásával járó infarktusméretet hatásosan csökkentenék. Ennek egyik magyarázata, hogy az I/R-t kísérő sejtelhalás összetett folyamata teljesen még nem tisztázott. A mechanizmus részletesebb megismerése javíthatja a kardioprotektív gyógyszerfejlesztések transzlálhatóságát. A klasszikus szabályozott (apoptózis, autofágia-mediálta sejthalál) és nem szabályozott (nekrózis) sejthalálfolyamatok mellett olyan programozott sejthalálformákat és mechanizmusokat ismertünk meg az elmúlt években, mint például a piroptózis, a PANoptózis vagy a ferroptózis. Jelen összefoglaló közleményünkben ezen folyamatokat kívánjuk röviden bemutatni a szív I/R károsodásában, valamint kitérünk a lehetséges modulálási stratégiákra is. LA - Hungarian DB - MTMT ER - TY - CONF AU - Szepesi, Ágnes AU - Pálfi, Péter AU - Kovács, Henrietta AU - Köhler, Zoltán Márton AU - Bakacsy, László AU - Zsigmond, Laura ED - Szepesi, Ágnes ED - Janda, Tibor TI - Polyamine catabolism and salt stress in plants T2 - 3rd Plant Polyamine Research Workshop. Program and Abstracts. SN - 9786150190716 PY - 2023 SP - 17 EP - 17 PG - 1 UR - https://m2.mtmt.hu/api/publication/34214220 ID - 34214220 LA - English DB - MTMT ER - TY - JOUR AU - Sonkodi, Balázs AU - Marsovszky, László AU - Csorba, Anita AU - Balog, Attila AU - Kopper, Bence AU - Keller-Pintér, Anikó AU - Nagy, Zoltán Zsolt AU - Resch, Miklós TI - Disrupted Neural Regeneration in Dry Eye Secondary to Ankylosing Spondylitis - With a Theoretical Link between Piezo2 Channelopathy and Gateway Reflex, WDR Neurons, and Flare-Ups JF - INTERNATIONAL JOURNAL OF MOLECULAR SCIENCES J2 - INT J MOL SCI VL - 24 PY - 2023 IS - 20 PG - 19 SN - 1661-6596 DO - 10.3390/ijms242015455 UR - https://m2.mtmt.hu/api/publication/34213807 ID - 34213807 N1 - Received: 24 September 2023 / Revised: 20 October 2023 / Accepted: 21 October 2023 / Published: 22 October 2023 AB - This study aimed at analyzing the corneal neural regeneration in ankylosing spondylitis patients using in vivo corneal confocal microscopy in correlation with Langerhans cell density, morphology, and dry eye parameters. Approximately 24 ankylosing spondylitis subjects and 35 age- and gender-matched control subjects were enrolled. Data analysis showed that all corneal nerve-fiber descriptives were lower in the ankylosing spondylitis group, implicating disrupted neural regeneration. Peripheral Langerhans cell density showed a negative correlation with nerve fiber descriptions. A negative correlation between tear film break-up time and corneal nerve fiber total branch density was detected. The potential role of somatosensory terminal Piezo2 channelopathy in the pathogenesis of dry eye disease and ankylosing spondylitis is highlighted in our study, exposing the neuroimmunological link between these diseases. We hypothesized earlier that spinal neuroimmune-induced sensitization due to this somatosensory terminal primary damage could lead to Langerhans cell activation in the cornea, in association with downregulated Piezo1 channels on these cells. This activation could lead to a Th17/Treg imbalance in dry eye secondary to ankylosing spondylitis. Hence, the corneal Piezo2 channelopathy-induced impaired Piezo2-Piezo1 crosstalk could explain the disrupted neural regeneration. Moreover, the translation of our findings highlights the link between Piezo2 channelopathy-induced gateway to pathophysiology and the gateway reflex, not to mention the potential role of spinal wide dynamic range neurons in the evolution of neuropathic pain and the flare-ups in ankylosing spondylitis and dry eye disease. LA - English DB - MTMT ER - TY - JOUR AU - Szűcs, Gergő AU - Pipicz, Márton AU - Szabó, Márton Richárd AU - Csont, Tamás Bálint AU - Török, László AU - Csonka, Csaba TI - Effect of Eccentric Exercise on Metabolic Health in Diabetes and Obesity JF - SPORTS MEDICINE-OPEN J2 - SPORT MED-OPEN VL - 9 PY - 2023 IS - 1 PG - 17 SN - 2199-1170 DO - 10.1186/s40798-023-00596-2 UR - https://m2.mtmt.hu/api/publication/34167864 ID - 34167864 AB - There is a growing body of evidence showing the importance of physical activity against civilization-induced metabolic diseases, including type 2 diabetes (T2DM) and obesity. Eccentric contraction, when skeletal muscles generate force by lengthening, is a unique type of skeletal muscle activity. Eccentric contraction may lead to better power production characteristics of the muscle because eccentric contraction requires less energy and can result in higher tension. Therefore, it is an ideal tool in the rehabilitation program of patients. However, the complex metabolic effect (i.e., fat mass reduction, increased lipid oxidation, improvement in blood lipid profile, and increased insulin sensitivity) of the eccentric contraction alone has scarcely been investigated. This paper aims to review the current literature to provide information on whether eccentric contraction can influence metabolic health and body composition in T2DM or obesity. We also discussed the potential role of myokines in mediating the effects of eccentric exercise. A better understanding of the mechanism of eccentric training and particularly their participation in the regulation of metabolic diseases may widen their possible therapeutic use and, thereby, may support the fight against the leading global risks for mortality in the world. LA - English DB - MTMT ER -