@article{MTMT:34757257,
	title = {Characterization of Skeletal Muscle Regeneration Revealed a Novel Growth Network Induced by Molecular Acupuncture-like Transfection},
	url = {https://m2.mtmt.hu/api/publication/34757257},
	author = {Zádor, Ernő},
	doi = {10.3390/biom14030363},
	journal-iso = {BIOMOLECULES},
	journal = {BIOMOLECULES},
	volume = {14},
	unique-id = {34757257},
	issn = {2218-273X},
	abstract = {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.},
	keywords = {regeneration; skeletal muscle; RAS; SERCA; in vivo transfection; molecular acupuncture},
	year = {2024},
	eissn = {2218-273X},
	orcid-numbers = {Zádor, Ernő/0000-0003-3029-6845}
}

@article{MTMT:34754547,
	title = {Paradoxical Effect of Caloric Restriction on Overload-Induced Muscle Growth in Diastolic Heart Failure},
	url = {https://m2.mtmt.hu/api/publication/34754547},
	author = {Zádor, Ernő},
	doi = {10.1016/j.jacbts.2023.11.011},
	journal-iso = {JACC-BASIC TRANSL SC},
	journal = {JACC:BASIC TO TRANSLATIONAL SCIENCE},
	volume = {9},
	unique-id = {34754547},
	issn = {2452-302X},
	year = {2024},
	eissn = {2452-302X},
	pages = {241-243},
	orcid-numbers = {Zádor, Ernő/0000-0003-3029-6845}
}

@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}
}

@article{MTMT:34435797,
	title = {Managing type 2 diabetes: targeting a microbial enzyme as a novel treatment option},
	url = {https://m2.mtmt.hu/api/publication/34435797},
	author = {Keller-Pintér, Anikó and Korcsmáros, Tamás and Vellai, Tibor},
	doi = {10.1038/s41392-023-01694-z},
	journal-iso = {SIGNAL TRANSDUCT TAR},
	journal = {SIGNAL TRANSDUCTION AND TARGETED THERAPY},
	volume = {8},
	unique-id = {34435797},
	issn = {2095-9907},
	year = {2023},
	eissn = {2059-3635},
	orcid-numbers = {Keller-Pintér, Anikó/0000-0002-4105-8458; Vellai, Tibor/0000-0002-3520-2572}
}

@article{MTMT:34416566,
	title = {Triptofán-származékok, mint lehetséges biomarkerek és terápiás célpontok egyes kardiovaszkuláris megbetegedésekben [Tryptophan metabolites as potential biomarkers and therapeutic targets in certain cardiovascular diseases]},
	url = {https://m2.mtmt.hu/api/publication/34416566},
	author = {Nógrádi-Halmi, Dóra and Erdélyi-Furka, Barbara Fanni and Molnár-Gáspár, Renáta and Csont, Tamás Bálint},
	doi = {10.26430/CHUNGARICA.2023.53.5.468},
	journal-iso = {CARDIOL HUNG},
	journal = {CARDIOLOGIA HUNGARICA},
	volume = {53},
	unique-id = {34416566},
	issn = {0133-5596},
	abstract = {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.},
	year = {2023},
	eissn = {1588-0230},
	pages = {468-475},
	orcid-numbers = {Nógrádi-Halmi, Dóra/0000-0001-9496-9354; Erdélyi-Furka, Barbara Fanni/0009-0005-7805-1910; Molnár-Gáspár, Renáta/0000-0001-9673-4532; Csont, Tamás Bálint/0000-0001-5792-2768}
}

@article{MTMT:34416562,
	title = {Piroptózis, PANoptózis és ferroptózis a szív iszkémia/reperfúziós károsodásában},
	url = {https://m2.mtmt.hu/api/publication/34416562},
	author = {Pipicz, Márton and Demján, Virág and Csonka, Csaba and Csont, Tamás Bálint},
	doi = {10.26430/CHUNGARICA.2023.53.5.451},
	journal-iso = {CARDIOL HUNG},
	journal = {CARDIOLOGIA HUNGARICA},
	volume = {53},
	unique-id = {34416562},
	issn = {0133-5596},
	abstract = {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.},
	year = {2023},
	eissn = {1588-0230},
	pages = {451-458},
	orcid-numbers = {Pipicz, Márton/0000-0002-0944-1684; Demján, Virág/0000-0002-6792-3024; Csonka, Csaba/0000-0003-2532-6261; Csont, Tamás Bálint/0000-0001-5792-2768}
}

@CONFERENCE{MTMT:34214220,
	title = {Polyamine catabolism and salt stress in plants},
	url = {https://m2.mtmt.hu/api/publication/34214220},
	author = {Szepesi, Ágnes and Pálfi, Péter and Kovács, Henrietta  and Köhler, Zoltán Márton and Bakacsy, László and Zsigmond, Laura},
	booktitle = {3rd Plant Polyamine Research Workshop. Program and Abstracts.},
	unique-id = {34214220},
	year = {2023},
	pages = {17-17},
	orcid-numbers = {Köhler, Zoltán Márton/0000-0002-8299-105X; Bakacsy, László/0000-0003-2593-1795; Zsigmond, Laura/0000-0002-1388-1762}
}

@article{MTMT:34213807,
	title = {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},
	url = {https://m2.mtmt.hu/api/publication/34213807},
	author = {Sonkodi, Balázs and Marsovszky, László and Csorba, Anita and Balog, Attila and Kopper, Bence and Keller-Pintér, Anikó and Nagy, Zoltán Zsolt and Resch, Miklós},
	doi = {10.3390/ijms242015455},
	journal-iso = {INT J MOL SCI},
	journal = {INTERNATIONAL JOURNAL OF MOLECULAR SCIENCES},
	volume = {24},
	unique-id = {34213807},
	issn = {1661-6596},
	abstract = {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.},
	year = {2023},
	eissn = {1422-0067},
	orcid-numbers = {Marsovszky, László/0000-0001-6463-8837; Csorba, Anita/0000-0002-3256-9440; Keller-Pintér, Anikó/0000-0002-4105-8458; Nagy, Zoltán Zsolt/0000-0002-7330-0464; Resch, Miklós/0000-0002-8285-1153}
}

@article{MTMT:34167864,
	title = {Effect of Eccentric Exercise on Metabolic Health in Diabetes and Obesity},
	url = {https://m2.mtmt.hu/api/publication/34167864},
	author = {Szűcs, Gergő and Pipicz, Márton and Szabó, Márton Richárd and Csont, Tamás Bálint and Török, László and Csonka, Csaba},
	doi = {10.1186/s40798-023-00596-2},
	journal-iso = {SPORT MED-OPEN},
	journal = {SPORTS MEDICINE-OPEN},
	volume = {9},
	unique-id = {34167864},
	issn = {2199-1170},
	abstract = {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.},
	year = {2023},
	eissn = {2198-9761},
	orcid-numbers = {Szűcs, Gergő/0000-0003-1874-2718; Pipicz, Márton/0000-0002-0944-1684; Szabó, Márton Richárd/0000-0003-0415-5192; Csont, Tamás Bálint/0000-0001-5792-2768; Csonka, Csaba/0000-0003-2532-6261}
}