@article{MTMT:37056978,
	title = {Knockout of the Intracellular Calcium Conducting Ion Channel Mitsugumin 23 (MG23) Protects Against Pressure Overload Induced Left Ventricular Hypertrophy and Cardiac Dysfunction},
	url = {https://m2.mtmt.hu/api/publication/37056978},
	author = {Dorward, Amy M. and Robertson, Gavin B. and Sneddon, Claire and Edel, Richard C. and O'Rourke, Chloe L. and Um, In Hwa and Harrison, David J. and Nishi, Miyuki and Takeshima, Hiroshi and Murdoch, Colin E. and Pitt, Samantha J.},
	doi = {10.1096/fj.202500832R},
	journal-iso = {FASEB J},
	journal = {FASEB JOURNAL},
	volume = {40},
	unique-id = {37056978},
	issn = {0892-6638},
	keywords = {HYPERTROPHY; Fibrosis; PRESSURE-OVERLOAD; Mitsugumin 23; SR Ca2+leak},
	year = {2026},
	eissn = {1530-6860},
	orcid-numbers = {Sneddon, Claire/0000-0001-9423-9175; Um, In Hwa/0000-0001-9999-4292}
}

@article{MTMT:36576276,
	title = {Increase in mechanical load and pro-fibrotic stimulation leads to fibrotic and hypertrophic remodeling in porcine living myocardial slices},
	url = {https://m2.mtmt.hu/api/publication/36576276},
	author = {Bentele, Marco and Linke, Sophie and Neumuller, Susanne and Korte, Andrea and Gietz, Anika and Just, Annette and Stucki-Koch, Angelika and Pfanne, Angelika and Liu, Junqing and Zhao, Jiahao and Schwennen, Cornelia and Homann, Christian and Visscher, Christian and Pflaum, Michael and Wiegmann, Bettina and Bar, Christian and Weber, Natalie and Fiedler, Jan and Thum, Thomas},
	doi = {10.1038/s41598-025-28222-z},
	journal-iso = {SCI REP},
	journal = {SCIENTIFIC REPORTS},
	volume = {15},
	unique-id = {36576276},
	year = {2025},
	eissn = {2045-2322}
}

@article{MTMT:36364220,
	title = {Cardio-oncology: Emerging Concepts in Cardiovascular Sequelae of Cancer Therapies, Translational Research and Reverse Cardio-oncology},
	url = {https://m2.mtmt.hu/api/publication/36364220},
	author = {Camilli, Massimiliano and Maggio, Luca and Tinti, Lorenzo and Torre, Ilaria and Viscovo, Marcello and Tamburrini, Giulia and Lombardo, Antonella and Cardinale, Daniela Maria and Minotti, Giorgio and Rocca, Bianca},
	doi = {10.15420/ecr.2024.49},
	journal-iso = {EUR CARDIOL},
	journal = {EUROPEAN CARDIOLOGY},
	volume = {20},
	unique-id = {36364220},
	issn = {1758-3756},
	year = {2025},
	eissn = {1758-3764},
	orcid-numbers = {Camilli, Massimiliano/0000-0002-2940-5349; Minotti, Giorgio/0000-0002-5678-6175; Rocca, Bianca/0000-0001-8304-6423}
}

@article{MTMT:36576281,
	title = {EPIDEMIOLOGICAL AND PATHOGENETIC ASPECTS OF CHRONIC HEART FAILURE IN PATIENTS WITH TYPE 2 DIABETES MELLITUS},
	url = {https://m2.mtmt.hu/api/publication/36576281},
	author = {Gorb, Yu.G. and Serik, S.A. and Tkachenko, O.V. and Ryabukha, V.V.},
	doi = {10.31718/2077-1096.25.2.300},
	journal-iso = {Act. Probl. of the Modern Med.},
	journal = {Актуальні проблеми сучасної медицини: Вісник Української медичної стоматологічної академії},
	volume = {25},
	unique-id = {36576281},
	issn = {2077-1096},
	year = {2025},
	eissn = {2077-1126},
	pages = {300-309}
}

@article{MTMT:36192574,
	title = {Tirzepatide, a dual GIP/GLP1-receptor co-agonist preserves cardiac function and improves survival in angiotensin II-induced heart failure model in mice: comparison to liraglutide},
	url = {https://m2.mtmt.hu/api/publication/36192574},
	author = {Hegedűs, Zsombor and Jakab, Márk and Gergely, Tamás G and Sayour, Viktor Nabil and Kovács, Andrea and Antal, Sára and Kovács, Tamás and Ferdinandy, Péter and Varga, Zoltán and Tóth, Viktória},
	doi = {10.1186/s12933-025-02806-5},
	journal-iso = {CARDIOVASC DIABETOL},
	journal = {CARDIOVASCULAR DIABETOLOGY},
	volume = {24},
	unique-id = {36192574},
	issn = {1475-2840},
	year = {2025},
	eissn = {1475-2840},
	orcid-numbers = {Jakab, Márk/0009-0004-8687-4311; Kovács, Tamás/0000-0003-4127-4545; Ferdinandy, Péter/0000-0002-6424-6806; Varga, Zoltán/0000-0002-2758-0784; Tóth, Viktória/0009-0003-9776-724X}
}

@article{MTMT:36223454,
	title = {Microgliosis, neuronal death, minor behavioral abnormalities and reduced endurance performance in alpha-ketoglutarate dehydrogenase complex deficient mice},
	url = {https://m2.mtmt.hu/api/publication/36223454},
	author = {Kokas, Márton and Budai, András and Kádár, Andrea and Mozaffaritabar, Soroosh and Zhou, Lei and Téglás, Tímea and Orova, Rebeka Sára and Gáspár, Dániel and Németh , Kristóf and Tóth, Dániel Márton and Sayour, Viktor Nabil and Kovácsházi, Csenger and Xue, Andrea and Szatmári, Réka Zsuzsanna and Törőcsik, Beáta and Máthé, Domokos and Stelczerné Kovács, Noémi and Szigeti, Krisztián and Nagy, Péter and Szatmári, Ildikó and Fekete, Csaba and Arányi, Tamás and Varga, Zoltán and Ferdinandy, Péter and Radák, Zsolt and Kozlov, Andrey V. and Tretter, László and Komlódi, Tímea and Ambrus, Attila},
	doi = {10.1016/j.redox.2025.103743},
	journal-iso = {REDOX BIOL},
	journal = {REDOX BIOLOGY},
	volume = {85},
	unique-id = {36223454},
	abstract = {The alpha-ketoglutarate dehydrogenase complex (KGDHc), also known as the 2-oxoglutarate dehydrogenase complex, plays a crucial role in oxidative metabolism. It catalyzes a key step in the tricarboxylic acid (TCA) cycle, producing NADH (primarily for oxidative phosphorylation) and succinyl-CoA (for substrate-level phosphorylation, among others). Additionally, KGDHc is also capable of generating reactive oxygen species, which contribute to mitochondrial oxidative stress. Hence, the KGDHc and its dysfunction are implicated in various pathological conditions, including selected neurodegenerative diseases. The pathological roles of KGDHc in these diseases are generally still obscure.
		The aim of this study was to assess whether the mitochondrial malfunctions observed in the dihydrolipoamide succinyltransferase (DLST) and dihydrolipoamide dehydrogenase (DLD) double heterozygous knockout (DLST+/--DLD+/-, DKO) mice are associated with neuronal and/or metabolic abnormalities.
		In the DKO animals, the mitochondrial O2 consumption and ATP production rates both decreased in a substrate-specific manner. Reduced H2O2 production was also observed, either due to Complex I inhibition with α-ketoglutarate or reverse electron transfer with succinate, which is significant in ischaemia-reperfusion injury. Middle-aged DKO mice exhibited minor cognitive decline, associated with microgliosis in the cerebral cortex and neuronal death in the Cornu Ammonis subfield 1 (CA1) of the hippocampus, indicating neuroinflammation. This was supported by increased levels of dynamin-related protein 1 (Drp1) and reduced levels of mitofusin 2 and peroxisome proliferator-activated receptor gamma coactivator 1-alpha (PGC-1α) in DKO mice. Observations on activity, food and oxygen consumption, and blood amino acid and acylcarnitine profiles revealed no significant differences. However, middle-aged DKO animals showed decreased performance in the treadmill fatigue-endurance test as compared to wild-type animals, accompanied by subtle resting cardiac impairment, but not skeletal muscle fibrosis.
		In conclusion, DKO animals compensate well the double-heterozygous knockout condition at the whole-body level with no major phenotypic changes under resting physiological conditions. However, under high energy demand, middle-aged DKO mice exhibited reduced performance, suggesting a decline in metabolic compensation. Additionally, microgliosis, neuronal death, decreased mitochondrial biogenesis, and altered mitochondrial dynamics were observed in DKO animals, resulting in minor cognitive decline. This is the first study to highlight the in vivo changes of this combined genetic modification. It demonstrates that unlike single knockout rodents, double knockout mice exhibit phenotypical alterations that worsen under stress situations.},
	keywords = {Alzheimer's disease; adenosine diphosphate; Membrane Potential, Mitochondrial; cognitive decline; Fatigue test; alpha-ketoglutarate; oxygen reactive species; Dihydrolipoyl succinyltransferase},
	year = {2025},
	eissn = {2213-2317},
	orcid-numbers = {Kokas, Márton/0000-0002-3982-4782; Budai, András/0000-0002-4634-2140; Mozaffaritabar, Soroosh/0000-0003-1052-7140; Zhou, Lei/0000-0002-8152-7896; Kovácsházi, Csenger/0000-0003-0283-9486; Törőcsik, Beáta/0000-0002-9838-3710; Nagy, Péter/0000-0003-3393-235X; Szatmári, Ildikó/0000-0003-1040-145X; Varga, Zoltán/0000-0002-2758-0784; Ferdinandy, Péter/0000-0002-6424-6806; Radák, Zsolt/0000-0003-1297-6804; Tretter, László/0000-0001-5638-2886; Komlódi, Tímea/0000-0001-9876-1411; Ambrus, Attila/0000-0001-6014-3175}
}

@article{MTMT:35575215,
	title = {Effects of sex and obesity on immune checkpoint inhibition-related cardiac systolic dysfunction in aged mice},
	url = {https://m2.mtmt.hu/api/publication/35575215},
	author = {Sayour, Viktor Nabil and Kucsera, Dániel and Alhaddad, Ayham Raed Noor and Tóth, Viktória and Gergely, Tamás G and Kovács, Tamás and Hegedűs, Zsombor and Jakab, Márk and Ferdinandy, Péter and Varga, Zoltán},
	doi = {10.1007/s00395-024-01088-4},
	journal-iso = {BASIC RES CARDIOL},
	journal = {BASIC RESEARCH IN CARDIOLOGY},
	volume = {120},
	unique-id = {35575215},
	issn = {0300-8428},
	abstract = {Despite accumulating data on underlying mechanisms, the influence of sex and prevalent cardio-metabolic co-morbidities on the manifestation and severity of immune checkpoint inhibitor (ICI)-induced cardiotoxicity has not been well defined. To elucidate whether sex and prevalent cardio-metabolic co-morbidities affect ICI-induced cardiotoxicity, we randomized 17-month-old male and female mice to receive control diet (CON) or high-fat diet (HFD) + L-NAME-a well-established mouse model of cardio-metabolic co-morbidities-for 17 weeks (n = 5-7), and evaluated markers of T-cell function in the spleen. As expected, HFD + L-NAME significantly increased body- and heart weight, and serum cholesterol levels, and caused no systolic dysfunction, however, led to diastolic dysfunction, cardiomyocyte hypertrophy, and increased fibrosis only in males compared to corresponding CON. Western blot analyses of splenic immune checkpoint protein levels showed differential expression depending on sex and prevalent cardio-metabolic co-morbidities, suggesting T-cell exhaustion in both sexes on HFD + L-NAME, but more pronounced in males. In a sub-study with a similar setup, we tested cardiotoxic manifestations of ICI by treating mice with anti-PD-1 monoclonal antibody (ICI) for the last 2 weeks of diet administration (n = 5-7). After 2 weeks of ICI treatment, cardiac systolic functions significantly decreased in CON, but not in HFD + L-NAME groups of both sexes compared to baseline (before ICI administration). In conclusion, in this exploratory study using aged mice, we describe for the first time that ICI-related systolic dysfunction is diminished in both sexes when obesity and hypercholesterolemia are present, possibly due to obesity-related T-cell exhaustion.},
	keywords = {SEX; OBESITY; cardiotoxicity; hypercholesterolemia; T-CELL EXHAUSTION; immune checkpoint inhibitor},
	year = {2025},
	eissn = {1435-1803},
	pages = {207-223},
	orcid-numbers = {Kucsera, Dániel/0000-0001-9446-847X; Tóth, Viktória/0009-0003-9776-724X; Kovács, Tamás/0000-0003-4127-4545; Jakab, Márk/0009-0004-8687-4311; Ferdinandy, Péter/0000-0002-6424-6806; Varga, Zoltán/0000-0002-2758-0784}
}

@article{MTMT:36487681,
	title = {Heart Failure in the Modern Era: A Narrative Overview of Recent Research from 2022–2025},
	url = {https://m2.mtmt.hu/api/publication/36487681},
	author = {Wilk, Michał and Tymków, Rafał},
	doi = {10.3390/jcdd12120484},
	journal-iso = {J CARDIOVASC DEV DIS},
	journal = {JOURNAL OF CARDIOVASCULAR DEVELOPMENT AND DISEASE},
	volume = {12},
	unique-id = {36487681},
	abstract = {Heart failure (HF) remains a major challenge in cardiovascular medicine, contributing to high global rates of hospitalization and mortality. Recent research (2022–2025) has emphasized its heterogeneity, highlighting distinct phenotypes—HFpEF, HFmrEF, and HFrEF—driven by mechanisms such as chronic inflammation, myocardial fibrosis, and neurohormonal imbalance. Advances in therapy, particularly with sodium–glucose cotransporter-2 inhibitors (SGLT2i), angiotensin receptor–neprilysin inhibitors (ARNI), and iron supplementation, have reshaped treatment strategies. Moreover, the growing recognition of overlaps between HF and cardiomyopathies such as hypertrophic, Takotsubo, and amyloidosis underscores the need for integrated care. This review summarizes recent findings from leading journals, mapping the evolving understanding of HF pathophysiology and management, and outlining emerging directions for research and clinical practice.},
	year = {2025},
	eissn = {2308-3425},
	orcid-numbers = {Wilk, Michał/0000-0002-3383-4357}
}