TY - JOUR AU - Dorward, Amy M. AU - Robertson, Gavin B. AU - Sneddon, Claire AU - Edel, Richard C. AU - O'Rourke, Chloe L. AU - Um, In Hwa AU - Harrison, David J. AU - Nishi, Miyuki AU - Takeshima, Hiroshi AU - Murdoch, Colin E. AU - Pitt, Samantha J. TI - Knockout of the Intracellular Calcium Conducting Ion Channel Mitsugumin 23 (MG23) Protects Against Pressure Overload Induced Left Ventricular Hypertrophy and Cardiac Dysfunction JF - FASEB JOURNAL J2 - FASEB J VL - 40 PY - 2026 IS - 2 PG - 16 SN - 0892-6638 DO - 10.1096/fj.202500832R UR - https://m2.mtmt.hu/api/publication/37056978 ID - 37056978 LA - English DB - MTMT ER - TY - JOUR AU - Bentele, Marco AU - Linke, Sophie AU - Neumuller, Susanne AU - Korte, Andrea AU - Gietz, Anika AU - Just, Annette AU - Stucki-Koch, Angelika AU - Pfanne, Angelika AU - Liu, Junqing AU - Zhao, Jiahao AU - Schwennen, Cornelia AU - Homann, Christian AU - Visscher, Christian AU - Pflaum, Michael AU - Wiegmann, Bettina AU - Bar, Christian AU - Weber, Natalie AU - Fiedler, Jan AU - Thum, Thomas TI - Increase in mechanical load and pro-fibrotic stimulation leads to fibrotic and hypertrophic remodeling in porcine living myocardial slices JF - SCIENTIFIC REPORTS J2 - SCI REP VL - 15 PY - 2025 IS - 1 SN - 2045-2322 DO - 10.1038/s41598-025-28222-z UR - https://m2.mtmt.hu/api/publication/36576276 ID - 36576276 N1 - Összes idézések száma a WoS-ban: 0 LA - English DB - MTMT ER - TY - JOUR AU - Camilli, Massimiliano AU - Maggio, Luca AU - Tinti, Lorenzo AU - Torre, Ilaria AU - Viscovo, Marcello AU - Tamburrini, Giulia AU - Lombardo, Antonella AU - Cardinale, Daniela Maria AU - Minotti, Giorgio AU - Rocca, Bianca TI - Cardio-oncology: Emerging Concepts in Cardiovascular Sequelae of Cancer Therapies, Translational Research and Reverse Cardio-oncology JF - EUROPEAN CARDIOLOGY J2 - EUR CARDIOL VL - 20 PY - 2025 PG - 7 SN - 1758-3756 DO - 10.15420/ecr.2024.49 UR - https://m2.mtmt.hu/api/publication/36364220 ID - 36364220 N1 - Összes idézések száma a WoS-ban: 0 LA - English DB - MTMT ER - TY - JOUR AU - Gorb, Yu.G. AU - Serik, S.A. AU - Tkachenko, O.V. AU - Ryabukha, V.V. TI - EPIDEMIOLOGICAL AND PATHOGENETIC ASPECTS OF CHRONIC HEART FAILURE IN PATIENTS WITH TYPE 2 DIABETES MELLITUS JF - Актуальні проблеми сучасної медицини: Вісник Української медичної стоматологічної академії J2 - Act. Probl. of the Modern Med. VL - 25 PY - 2025 IS - 2 SP - 300 EP - 309 PG - 10 SN - 2077-1096 DO - 10.31718/2077-1096.25.2.300 UR - https://m2.mtmt.hu/api/publication/36576281 ID - 36576281 N1 - Összes idézések száma a WoS-ban: 0 LA - Russian DB - MTMT ER - TY - JOUR AU - Hegedűs, Zsombor AU - Jakab, Márk AU - Gergely, Tamás G AU - Sayour, Viktor Nabil AU - Kovács, Andrea AU - Antal, Sára AU - Kovács, Tamás AU - Ferdinandy, Péter AU - Varga, Zoltán AU - Tóth, Viktória TI - 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 JF - CARDIOVASCULAR DIABETOLOGY J2 - CARDIOVASC DIABETOL VL - 24 PY - 2025 IS - 1 PG - 16 SN - 1475-2840 DO - 10.1186/s12933-025-02806-5 UR - https://m2.mtmt.hu/api/publication/36192574 ID - 36192574 N1 - Export Date: 07 July 2025; Correspondence Address: V.E. Tóth; Department of Pharmacology and Pharmacotherapy, Semmelweis University, Budapest, Hungary; email: toth.viktoria@semmelweis.hu; CODEN: CDAIA LA - English DB - MTMT ER - TY - JOUR AU - Kokas, Márton AU - Budai, András AU - Kádár, Andrea AU - Mozaffaritabar, Soroosh AU - Zhou, Lei AU - Téglás, Tímea AU - Orova, Rebeka Sára AU - Gáspár, Dániel AU - Németh , Kristóf AU - Tóth, Dániel Márton AU - Sayour, Viktor Nabil AU - Kovácsházi, Csenger AU - Xue, Andrea AU - Szatmári, Réka Zsuzsanna AU - Törőcsik, Beáta AU - Máthé, Domokos AU - Stelczerné Kovács, Noémi AU - Szigeti, Krisztián AU - Nagy, Péter AU - Szatmári, Ildikó AU - Fekete, Csaba AU - Arányi, Tamás AU - Varga, Zoltán AU - Ferdinandy, Péter AU - Radák, Zsolt AU - Kozlov, Andrey V. AU - Tretter, László AU - Komlódi, Tímea AU - Ambrus, Attila TI - Microgliosis, neuronal death, minor behavioral abnormalities and reduced endurance performance in alpha-ketoglutarate dehydrogenase complex deficient mice JF - REDOX BIOLOGY J2 - REDOX BIOL VL - 85 PY - 2025 PG - 19 SN - 2213-2317 DO - 10.1016/j.redox.2025.103743 UR - https://m2.mtmt.hu/api/publication/36223454 ID - 36223454 AB - 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. LA - English DB - MTMT ER - TY - JOUR AU - Sayour, Viktor Nabil AU - Kucsera, Dániel AU - Alhaddad, Ayham Raed Noor AU - Tóth, Viktória AU - Gergely, Tamás G AU - Kovács, Tamás AU - Hegedűs, Zsombor AU - Jakab, Márk AU - Ferdinandy, Péter AU - Varga, Zoltán TI - Effects of sex and obesity on immune checkpoint inhibition-related cardiac systolic dysfunction in aged mice JF - BASIC RESEARCH IN CARDIOLOGY J2 - BASIC RES CARDIOL VL - 120 PY - 2025 IS - 1 SP - 207 EP - 223 PG - 17 SN - 0300-8428 DO - 10.1007/s00395-024-01088-4 UR - https://m2.mtmt.hu/api/publication/35575215 ID - 35575215 N1 - *Nabil V. Sayour and Dániel Kucsera have contributed to this work equally. AB - 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. LA - English DB - MTMT ER - TY - JOUR AU - Wilk, Michał AU - Tymków, Rafał TI - Heart Failure in the Modern Era: A Narrative Overview of Recent Research from 2022–2025 JF - JOURNAL OF CARDIOVASCULAR DEVELOPMENT AND DISEASE J2 - J CARDIOVASC DEV DIS VL - 12 PY - 2025 IS - 12 SN - 2308-3425 DO - 10.3390/jcdd12120484 UR - https://m2.mtmt.hu/api/publication/36487681 ID - 36487681 N1 - Funding Agency and Grant Number: Wroclaw Medical University; Wroclaw Medical University, Poland [IDUB.A46B.24.002] Funding text: This research was funded by a grant from Wroclaw Medical University, Poland, number IDUB.A46B.24.002. The presented research results were funded by the Development Strategy of the Wroclaw Medical University entitled "UMW in the Light of Scientific Excellence 2024-2026." AB - 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. LA - English DB - MTMT ER -