@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}
}

@article{MTMT:34008336,
	title = {The effect of electrical stimulation of skeletal muscle on cardioprotection and on muscle-derived myokine levels in rats: A pilot study},
	url = {https://m2.mtmt.hu/api/publication/34008336},
	author = {Szabó, Márton Richárd and Csont, Tamás Bálint and Csonka, Csaba},
	doi = {10.1556/2060.2023.00198},
	journal-iso = {PHYSIOL INT},
	journal = {PHYSIOLOGY INTERNATIONAL},
	volume = {110},
	unique-id = {34008336},
	issn = {2498-602X},
	abstract = {Electrical muscle stimulation (EMS) is a widely used method in sports and rehabilitation therapies to simulate physical exercise. EMS treatment via skeletal muscle activity improves the cardiovascular functions and the overall physical condition of the patients. However, the cardioprotective effect of EMS has not been proven so far, therefore, the aim of this study was to investigate the potential cardiac conditioning effect of EMS in an animal model. Low-frequency 35-min EMS was applied to the gastrocnemius muscle of male Wistar rats for three consecutive days. Their isolated hearts were then subjected to 30 min global ischemia and 120 min reperfusion. At the end of reperfusion cardiac specific creatine kinase (CK-MB) and lactate dehydrogenase (LDH) enzyme release and myocardial infarct size were determined. Additionally, skeletal muscle-driven myokine expression and release were also assessed. Phosphorylation of cardioprotective signaling pathway members AKT, ERK1/2, and STAT3 proteins were also measured. EMS significantly attenuated cardiac LDH and CK-MB enzyme activities in the coronary effluents at the end of the ex vivo reperfusion. EMS treatment considerably altered the myokine content of the stimulated gastrocnemius muscle without altering circulating myokine levels in the serum. Additionally, phosphorylation of cardiac AKT, ERK1/2, and STAT3 was not significantly different in the two groups. Despite the lack of significant infarct size reduction, the EMS treatment seems to influence the course of cellular damage due to ischemia/reperfusion and favorably modifies skeletal muscle myokine expressions. Our results suggest that EMS may have a protective effect on the myocardium, however, further optimization is required.},
	year = {2023},
	eissn = {2677-0164},
	pages = {135-149},
	orcid-numbers = {Szabó, Márton Richárd/0000-0003-0415-5192; Csont, Tamás Bálint/0000-0001-5792-2768; Csonka, Csaba/0000-0003-2532-6261}
}

@article{MTMT:33322061,
	title = {Acetylation State of Lysine 14 of Histone H3.3 Affects Mutant Huntingtin Induced Pathogenesis},
	url = {https://m2.mtmt.hu/api/publication/33322061},
	author = {Faragó, Anikó and Zsindely, Nóra and Farkas, Anita and Neller, Alexandra and Siági, Fruzsina and Szabó, Márton Richárd and Csont, Tamás Bálint and Bodai, László},
	doi = {10.3390/ijms232315173},
	journal-iso = {INT J MOL SCI},
	journal = {INTERNATIONAL JOURNAL OF MOLECULAR SCIENCES},
	volume = {23},
	unique-id = {33322061},
	issn = {1661-6596},
	abstract = {Huntington’s Disease (HD) is a fatal neurodegenerative disorder caused by the expansion of a polyglutamine-coding CAG repeat in the Huntingtin gene. One of the main causes of neurodegeneration in HD is transcriptional dysregulation that, in part, is caused by the inhibition of histone acetyltransferase (HAT) enzymes. HD pathology can be alleviated by increasing the activity of specific HATs or by inhibiting histone deacetylase (HDAC) enzymes. To determine which histone’s post-translational modifications (PTMs) might play crucial roles in HD pathology, we investigated the phenotype-modifying effects of PTM mimetic mutations of variant histone H3.3 in a Drosophila model of HD. Specifically, we studied the mutations (K→Q: acetylated; K→R: non-modified; and K→M: methylated) of lysine residues K9, K14, and K27 of transgenic H3.3. In the case of H3.3K14Q modification, we observed the amelioration of all tested phenotypes (viability, longevity, neurodegeneration, motor activity, and circadian rhythm defects), while H3.3K14R had the opposite effect. H3.3K14Q expression prevented the negative effects of reduced Gcn5 (a HAT acting on H3K14) on HD pathology, while it only partially hindered the positive effects of heterozygous Sirt1 (an HDAC acting on H3K14). Thus, we conclude that the Gcn5-dependent acetylation of H3.3K14 might be an important epigenetic contributor to HD pathology.},
	year = {2022},
	eissn = {1422-0067},
	orcid-numbers = {Zsindely, Nóra/0000-0002-6189-3100; Szabó, Márton Richárd/0000-0003-0415-5192; Csont, Tamás Bálint/0000-0001-5792-2768; Bodai, László/0000-0001-8411-626X}
}

@article{MTMT:32924828,
	title = {Diet-Induced Hypercholesterolemia Leads to Cardiac Dysfunction and Alterations in the Myocardial Proteome},
	url = {https://m2.mtmt.hu/api/publication/32924828},
	author = {Szabó, Márton Richárd and Pipicz, Márton and Sárközy, Márta and Bruszel, Bella and Szabó, Zoltán and Csont, Tamás Bálint},
	doi = {10.3390/ijms23137387},
	journal-iso = {INT J MOL SCI},
	journal = {INTERNATIONAL JOURNAL OF MOLECULAR SCIENCES},
	volume = {23},
	unique-id = {32924828},
	issn = {1661-6596},
	abstract = {Elevated blood cholesterol is a major risk factor for coronary heart disease. Moreover, direct effects on the myocardium also contribute to the adverse effects of hypercholesterolemia. Here, we investigated the effect of hypercholesterolemia on the cardiac proteome. Male Wistar rats were fed with a laboratory rodent chow supplemented with 2% cholesterol for 8 weeks to induce hypercholesterolemia. The protein expression data obtained from the proteomic characterization of left ventricular samples from normo- and hypercholesterolemic animals were subjected to gene ontology (GO) and protein interaction analyses. Elevated circulating cholesterol levels were accompanied by diastolic dysfunction in cholesterol-fed rats. The proteomic characterization of left ventricular samples revealed altered expression of 45 proteins due to hypercholesterolemia. Based on the Gene Ontology analysis, hypercholesterolemia was associated with disturbed expression of cytoskeletal and contractile proteins. Beta-actin was downregulated in the hypercholesterolemic myocardium, and established a prominent hub of the protein interaction network. Analysis of the unfiltered dataset revealed concordant downregulated expression patterns in proteins associated with the arrangement of the contractile system (e.g., cardiac-specific troponins and myosin complex), and in subunits of the mitochondrial respiratory chain. We conclude that the observed changes in the cardiac proteome may contribute to the development of diastolic dysfunction in hypercholesterolemia.},
	year = {2022},
	eissn = {1422-0067},
	orcid-numbers = {Szabó, Márton Richárd/0000-0003-0415-5192; Pipicz, Márton/0000-0002-0944-1684; Sárközy, Márta/0000-0002-5929-2146; Szabó, Zoltán/0000-0001-8278-8038; Csont, Tamás Bálint/0000-0001-5792-2768}
}

@article{MTMT:32191180,
	title = {Ischemic preconditioning protects the heart against ischemia-reperfusion injury in chronic kidney disease in both males and females},
	url = {https://m2.mtmt.hu/api/publication/32191180},
	author = {Sárközy, Márta and Márványkövi, Fanni and Szűcs, Gergő and Kovács, Zsuzsanna and Szabó, Márton Richárd and Molnár-Gáspár, Renáta and Siska, Andrea and Kővári, Bence and Cserni, Gábor and Földesi, Imre and Csont, Tamás Bálint},
	doi = {10.1186/s13293-021-00392-1},
	journal-iso = {BIOL SEX DIFFER},
	journal = {BIOLOGY OF SEX DIFFERENCES},
	volume = {12},
	unique-id = {32191180},
	year = {2021},
	eissn = {2042-6410},
	orcid-numbers = {Sárközy, Márta/0000-0002-5929-2146; Márványkövi, Fanni/0000-0002-5114-1319; Szűcs, Gergő/0000-0003-1874-2718; Kovács, Zsuzsanna/0000-0002-4197-4579; Szabó, Márton Richárd/0000-0003-0415-5192; Molnár-Gáspár, Renáta/0000-0001-9673-4532; Kővári, Bence/0000-0002-4498-8781; Cserni, Gábor/0000-0003-1344-7744; Földesi, Imre/0000-0002-3329-8136; Csont, Tamás Bálint/0000-0001-5792-2768}
}

@article{MTMT:32048186,
	title = {Correlated Motions of Conserved Polar Motifs Lay out a Plausible Mechanism of G Protein-Coupled Receptor Activation},
	url = {https://m2.mtmt.hu/api/publication/32048186},
	author = {Mitra, Argha and Sarkar, Arijit and Szabó, Márton Richárd and Borics, Attila},
	doi = {10.3390/biom11050670},
	journal-iso = {BIOMOLECULES},
	journal = {BIOMOLECULES},
	volume = {11},
	unique-id = {32048186},
	issn = {2218-273X},
	abstract = {Recent advancements in the field of experimental structural biology have provided high-resolution structures of active and inactive state G protein-coupled receptors (GPCRs), a highly important pharmaceutical target family, but the process of transition between these states is poorly understood. According to the current theory, GPCRs exist in structurally distinct, dynamically interconverting functional states of which populations are shifted upon binding of ligands and intracellular signaling proteins. However, explanation of the activation mechanism, on an entirely structural basis, gets complicated when multiple activation pathways and active receptor states are considered. Our unbiased, atomistic molecular dynamics simulations of the mu opioid receptor (MOP) revealed that transmission of external stimulus to the intracellular surface of the receptor is accompanied by subtle, concerted movements of highly conserved polar amino acid side chains along the 7th transmembrane helix. This may entail the rearrangement of polar species and the shift of macroscopic polarization in the transmembrane domain, triggered by agonist binding. Based on our observations and numerous independent indications, we suggest amending the widely accepted theory that the initiation event of GPCR activation is the shift of macroscopic polarization between the ortho- and allosteric binding pockets and the intracellular G protein-binding interface.},
	year = {2021},
	eissn = {2218-273X},
	orcid-numbers = {Szabó, Márton Richárd/0000-0003-0415-5192}
}

@article{MTMT:31623181,
	title = {Androstano-arylpyrimidines. novel small molecule inhibitors of MDR1 for sensitizing multidrug-resistant breast cancer cells},
	url = {https://m2.mtmt.hu/api/publication/31623181},
	author = {Gopisetty, Mohana Krishna and Adamecz, Dóra Izabella and Nagy, Ferenc István and Baji, Ádám and Lathira, Vasiliki and Szabó, Márton Richárd and Molnár-Gáspár, Renáta and Csont, Tamás Bálint and Nagyné Frank, Éva and Csontné Kiricsi, Mónika},
	doi = {10.1016/j.ejps.2020.105587},
	journal-iso = {EUR J PHARM SCI},
	journal = {EUROPEAN JOURNAL OF PHARMACEUTICAL SCIENCES},
	volume = {156},
	unique-id = {31623181},
	issn = {0928-0987},
	year = {2021},
	eissn = {1879-0720},
	orcid-numbers = {Gopisetty, Mohana Krishna/0000-0002-4310-3478; Adamecz, Dóra Izabella/0000-0002-1883-9600; Szabó, Márton Richárd/0000-0003-0415-5192; Molnár-Gáspár, Renáta/0000-0001-9673-4532; Csont, Tamás Bálint/0000-0001-5792-2768; Nagyné Frank, Éva/0000-0002-1332-0551; Csontné Kiricsi, Mónika/0000-0002-8416-2052}
}

@article{MTMT:31789683,
	title = {Modulatory effect of myokines on reactive oxygen species in ischemia/reperfusion},
	url = {https://m2.mtmt.hu/api/publication/31789683},
	author = {Szabó, Márton Richárd and Pipicz, Márton and Csont, Tamás Bálint and Csonka, Csaba},
	doi = {10.3390/ijms21249382},
	journal-iso = {INT J MOL SCI},
	journal = {INTERNATIONAL JOURNAL OF MOLECULAR SCIENCES},
	volume = {21},
	unique-id = {31789683},
	issn = {1661-6596},
	abstract = {There is a growing body of evidence showing the importance of physical activity against acute ischemic events in various organs. Ischemia/reperfusion injury (I/R) is characterized by tissue damage as a result of restriction and subsequent restoration of blood supply to an organ. Oxidative stress due to increased reactive oxygen species formation and/or insufficient antioxidant defense is considered to play an important role in I/R. Physical activity not only decreases the general risk factors for ischemia but also confers direct anti-ischemic protection via myokine production. Myokines are skeletal muscle-derived cytokines, representing multifunctional communication channels between the contracting skeletal muscle and other organs through an endocrine manner. In this review, we discuss the most prominent members of the myokines (i.e., brain-derived neurotrophic factor (BDNF), cathepsin B, decorin, fibroblast growth factors-2 and-21, follistatin, follistatin-like, insulin-like growth factor-1; interleukin-6, interleukin-7, interleukin-15, irisin, leukemia inhibitory factor, meteorin-like, myonectin, musclin, myostatin, and osteoglycin) with a particular interest in their potential influence on reactive oxygen and nitrogen species formation or antioxidant capacity. A better understanding of the mechanism of action of myokines and particularly their participation in the regulation of oxidative stress may widen their possible therapeutic use and, thereby, may support the fight against I/R. © 2020 by the authors. Licensee MDPI, Basel, Switzerland.},
	keywords = {Exercise; FGF; cardioprotection; conditioning; ROS; LIF; Myocardial; Remote; IGF},
	year = {2020},
	eissn = {1422-0067},
	orcid-numbers = {Szabó, Márton Richárd/0000-0003-0415-5192; Pipicz, Márton/0000-0002-0944-1684; Csont, Tamás Bálint/0000-0001-5792-2768; Csonka, Csaba/0000-0003-2532-6261}
}

@{MTMT:31647861,
	title = {Development of diet-induced hypercholesterolemia is associated with alterations in cardiac gene expression profile},
	url = {https://m2.mtmt.hu/api/publication/31647861},
	author = {Szabó, Márton Richárd and Molnár-Gáspár, Renáta and Pipicz, Márton and Zsindely, Nóra and Diószegi, Petra and Sárközy, Márta and Bodai, László and Csont, Tamás Bálint},
	booktitle = {Proceedings of the EFOP-3.6.2-16-2017-00006 (LIVE LONGER) project},
	unique-id = {31647861},
	year = {2020},
	pages = {72-72},
	orcid-numbers = {Szabó, Márton Richárd/0000-0003-0415-5192; Molnár-Gáspár, Renáta/0000-0001-9673-4532; Pipicz, Márton/0000-0002-0944-1684; Zsindely, Nóra/0000-0002-6189-3100; Diószegi, Petra/0000-0001-8109-2266; Sárközy, Márta/0000-0002-5929-2146; Bodai, László/0000-0001-8411-626X; Csont, Tamás Bálint/0000-0001-5792-2768}
}

@article{MTMT:31330253,
	title = {Hypercholesterolemia Interferes with Induction of miR-125b-1-3p in Preconditioned Hearts},
	url = {https://m2.mtmt.hu/api/publication/31330253},
	author = {Szabó, Márton Richárd and Molnár-Gáspár, Renáta and Pipicz, Márton and Zsindely, Nóra and Diószegi, Petra and Sárközy, Márta and Bodai, László and Csont, Tamás Bálint},
	doi = {10.3390/ijms21113744},
	journal-iso = {INT J MOL SCI},
	journal = {INTERNATIONAL JOURNAL OF MOLECULAR SCIENCES},
	volume = {21},
	unique-id = {31330253},
	issn = {1661-6596},
	year = {2020},
	eissn = {1422-0067},
	orcid-numbers = {Szabó, Márton Richárd/0000-0003-0415-5192; Molnár-Gáspár, Renáta/0000-0001-9673-4532; Pipicz, Márton/0000-0002-0944-1684; Zsindely, Nóra/0000-0002-6189-3100; Diószegi, Petra/0000-0001-8109-2266; Sárközy, Márta/0000-0002-5929-2146; Bodai, László/0000-0001-8411-626X; Csont, Tamás Bálint/0000-0001-5792-2768}
}