@article{MTMT:34799327,
	title = {NASH triggers cardiometabolic HFpEF in aging mice},
	url = {https://m2.mtmt.hu/api/publication/34799327},
	author = {Kucsera, Dániel and Ruppert, Mihály and Sayour, Viktor Nabil and Tóth, Viktória and Kovács, Tamás and Hegedűs, Zsombor and Onódi, Zsófia and Fábián, Alexandra and Kovács, Attila and Radovits, Tamás and Merkely, Béla Péter and Pacher, Pál and Ferdinandy, Péter and Varga, Zoltán},
	doi = {10.1007/s11357-024-01153-9},
	journal-iso = {GEROSCIENCE},
	journal = {GEROSCIENCE: OFFICIAL JOURNAL OF THE AMERICAN AGING ASSOCIATION (AGE)},
	volume = {In press},
	unique-id = {34799327},
	issn = {2509-2715},
	abstract = {Both heart failure with preserved ejection fraction (HFpEF) and non-alcoholic fatty liver disease (NAFLD) develop due to metabolic dysregulation, has similar risk factors (e.g., insulin resistance, systemic inflammation) and are unresolved clinical challenges. Therefore, the potential link between the two disease is important to study. We aimed to evaluate whether NASH is an independent factor of cardiac dysfunction and to investigate the age dependent effects of NASH on cardiac function. C57Bl/6 J middle aged (10 months old) and aged mice (24 months old) were fed either control or choline deficient (CDAA) diet for 8 weeks. Before termination, echocardiography was performed. Upon termination, organ samples were isolated for histological and molecular analysis. CDAA diet led to the development of NASH in both age groups, without inducing weight gain, allowing to study the direct effect of NASH on cardiac function. Mice with NASH developed hepatomegaly, fibrosis, and inflammation. Aged animals had increased heart weight. Conventional echocardiography revealed normal systolic function in all cohorts, while increased left ventricular volumes in aged mice. Two-dimensional speckle tracking echocardiography showed subtle systolic and diastolic deterioration in aged mice with NASH. Histologic analyses of cardiac samples showed increased cross-sectional area, pronounced fibrosis and Col1a1 gene expression, and elevated intracardiac CD68 + macrophage count with increased Il1b expression. Conventional echocardiography failed to reveal subtle change in myocardial function; however, 2D speckle tracking echocardiography was able to identify diastolic deterioration. NASH had greater impact on aged animals resulting in cardiac hypertrophy, fibrosis, and inflammation.},
	year = {2024},
	eissn = {2509-2723},
	orcid-numbers = {Kucsera, Dániel/0000-0001-9446-847X; Tóth, Viktória/0000-0002-0426-2425; Kovács, Tamás/0000-0003-4127-4545; Onódi, Zsófia/0000-0002-3746-8016; Fábián, Alexandra/0000-0002-8449-0638; Kovács, Attila/0000-0003-2320-6434; Merkely, Béla Péter/0000-0001-6514-0723; Pacher, Pál/0000-0001-7036-8108; Ferdinandy, Péter/0000-0002-6424-6806; Varga, Zoltán/0000-0002-2758-0784}
}

@article{MTMT:34724783,
	title = {Heart failure pharmacotherapy and cancer: pathways and pre-clinical/clinical evidence},
	url = {https://m2.mtmt.hu/api/publication/34724783},
	author = {Sayour, Viktor Nabil and Paál, Ágnes and Ameri, Pietro and Meijers, Wouter C and Minotti, Giorgio and Andreadou, Ioanna and Lombardo, Antonella and Camilli, Massimiliano and Drexel, Heinz and Grove, Erik Lerkevang and Dan, Gheorghe Andrei and Ivanescu, Andreea and Semb, Anne Grete and Savarese, Gianluigi and Dobrev, Dobromir and Crea, Filippo and Kaski, Juan-Carlos and de Boer, Rudolf A and Ferdinandy, Péter and Varga, Zoltán},
	doi = {10.1093/eurheartj/ehae105},
	journal-iso = {EUR HEART J},
	journal = {EUROPEAN HEART JOURNAL},
	volume = {45},
	unique-id = {34724783},
	issn = {0195-668X},
	abstract = {Heart failure (HF) patients have a significantly higher risk of new-onset cancer and cancer-associated mortality, compared to subjects free of HF. While both the prevention and treatment of new-onset HF in patients with cancer have been investigated extensively, less is known about the prevention and treatment of new-onset cancer in patients with HF, and whether and how guideline-directed medical therapy (GDMT) for HF should be modified when cancer is diagnosed in HF patients. The purpose of this review is to elaborate and discuss the effects of pillar HF pharmacotherapies, as well as digoxin and diuretics on cancer, and to identify areas for further research and novel therapeutic strategies. To this end, in this review, (i) proposed effects and mechanisms of action of guideline-directed HF drugs on cancer derived from pre-clinical data will be described, (ii) the evidence from both observational studies and randomized controlled trials on the effects of guideline-directed medical therapy on cancer incidence and cancer-related outcomes, as synthetized by meta-analyses will be reviewed, and (iii) considerations for future pre-clinical and clinical investigations will be provided.},
	year = {2024},
	eissn = {1522-9645},
	pages = {1224-1240},
	orcid-numbers = {Paál, Ágnes/0000-0003-2292-3714; Minotti, Giorgio/0000-0002-5678-6175; Camilli, Massimiliano/0000-0002-2940-5349; Dobrev, Dobromir/0000-0002-4612-117X; Kaski, Juan-Carlos/0000-0001-8068-0189; de Boer, Rudolf A/0000-0002-4775-9140; Ferdinandy, Péter/0000-0002-6424-6806; Varga, Zoltán/0000-0002-2758-0784}
}

@article{MTMT:34538456,
	title = {Immune checkpoints in cardiac physiology and pathology: therapeutic targets for heart failure},
	url = {https://m2.mtmt.hu/api/publication/34538456},
	author = {Gergely, Tamás G and Drobni, Zsófia and Kallikourdis, Marinos and Zhu, Han and Meijers, Wouter C. and Neilan, Tomas G. and Rassaf, Tienush and Ferdinandy, Péter and Varga, Zoltán},
	doi = {10.1038/s41569-023-00986-9},
	journal-iso = {NAT REV CARDIOL},
	journal = {NATURE REVIEWS CARDIOLOGY},
	unique-id = {34538456},
	issn = {1759-5002},
	year = {2024},
	eissn = {1759-5010},
	orcid-numbers = {Drobni, Zsófia/0000-0002-1355-5318; Zhu, Han/0000-0002-2751-7814; Neilan, Tomas G./0000-0003-4356-8176; Ferdinandy, Péter/0000-0002-6424-6806; Varga, Zoltán/0000-0002-2758-0784}
}

@article{MTMT:34474992,
	title = {YB-1 Is a Novel Target for the Inhibition of α-Adrenergic-Induced Hypertrophy},
	url = {https://m2.mtmt.hu/api/publication/34474992},
	author = {Heger, Jacqueline and Partsch, Stefan and Harjung, Claudia and Varga, Zoltán and Baranyai, Tamás and Weiß, Johannes and Kremer, Lea and Locquet, Fabian and Leszek, Przemyslaw and Ágg, Bence and Benczik, Bettina and Ferdinandy, Péter and Schulz, Rainer and Euler, Gerhild},
	doi = {10.3390/ijms25010401},
	journal-iso = {INT J MOL SCI},
	journal = {INTERNATIONAL JOURNAL OF MOLECULAR SCIENCES},
	volume = {25},
	unique-id = {34474992},
	issn = {1661-6596},
	abstract = {Cardiac hypertrophy resulting from sympathetic nervous system activation triggers the development of heart failure. The transcription factor Y-box binding protein 1 (YB-1) can interact with transcription factors involved in cardiac hypertrophy and may thereby interfere with the hypertrophy growth process. Therefore, the question arises as to whether YB-1 influences cardiomyocyte hypertrophy and might thereby influence the development of heart failure. YB-1 expression is downregulated in human heart biopsies of patients with ischemic cardiomyopathy (n = 8), leading to heart failure. To study the impact of reduced YB-1 in cardiac cells, we performed small interfering RNA (siRNA) experiments in H9C2 cells as well as in adult cardiomyocytes (CMs) of rats. The specificity of YB-1 siRNA was analyzed by a miRNA-like off-target prediction assay identifying potential genes. Testing three high-scoring genes by transfecting cardiac cells with YB-1 siRNA did not result in downregulation of these genes in contrast to YB-1, whose downregulation increased hypertrophic growth. Hypertrophic growth was mediated by PI3K under PE stimulation, as well by downregulation with YB-1 siRNA. On the other hand, overexpression of YB-1 in CMs, caused by infection with an adenovirus encoding YB-1 (AdYB-1), prevented hypertrophic growth under α-adrenergic stimulation with phenylephrine (PE), but not under stimulation with growth differentiation factor 15 (GDF15; n = 10–16). An adenovirus encoding the green fluorescent protein (AdGFP) served as the control. YB-1 overexpression enhanced the mRNA expression of the Gq inhibitor regulator of G-protein signaling 2 (RGS2) under PE stimulation (n = 6), potentially explaining its inhibitory effect on PE-induced hypertrophic growth. This study shows that YB-1 protects cardiomyocytes against PE-induced hypertrophic growth. Like in human end-stage heart failure, YB-1 downregulation may cause the heart to lose its protection against hypertrophic stimuli and progress to heart failure. Therefore, the transcription factor YB-1 is a pivotal signaling molecule, providing perspectives for therapeutic approaches.},
	year = {2024},
	eissn = {1422-0067},
	orcid-numbers = {Varga, Zoltán/0000-0002-2758-0784; Baranyai, Tamás/0000-0002-9378-8938; Ágg, Bence/0000-0002-6492-0426; Benczik, Bettina/0000-0003-0379-2181; Ferdinandy, Péter/0000-0002-6424-6806; Schulz, Rainer/0000-0003-3017-0476; Euler, Gerhild/0000-0001-9094-773X}
}

@article{MTMT:34213292,
	title = {A dual role of lysophosphatidic acid type 2 receptor (LPAR2) in nonsteroidal anti-inflammatory drug-induced mouse enteropathy},
	url = {https://m2.mtmt.hu/api/publication/34213292},
	author = {Hutka, Barbara and Várallyay, Anett and László, Szilvia Bianka and Tóth, András Sebestyén and Scheich, Bálint and Paku, Sándor and Vörös, Imre and Pós, Zoltán and Varga, Zoltán and Norman, Derek D. and Balogh, Andrea and Benyó, Zoltán and Tigyi, Gabor and Gyires, Klára and Zádori, Zoltán Sándor},
	doi = {10.1038/s41401-023-01175-7},
	journal-iso = {ACTA PHARMACOL SIN},
	journal = {ACTA PHARMACOLOGICA SINICA},
	volume = {45},
	unique-id = {34213292},
	issn = {1671-4083},
	abstract = {Lysophosphatidic acid (LPA) is a bioactive phospholipid mediator that has been found to ameliorate nonsteroidal anti-inflammatory drug (NSAID)-induced gastric injury by acting on lysophosphatidic acid type 2 receptor (LPAR2). In this study, we investigated whether LPAR2 signaling was implicated in the development of NSAID-induced small intestinal injury (enteropathy), another major complication of NSAID use. Wild-type (WT) and Lpar2 deficient ( Lpar2 −/− ) mice were treated with a single, large dose (20 or 30 mg/kg, i.g.) of indomethacin (IND). The mice were euthanized at 6 or 24 h after IND treatment. We showed that IND-induced mucosal enteropathy and neutrophil recruitment occurred much earlier (at 6 h after IND treatment) in Lpar2 −/− mice compared to WT mice, but the tissue levels of inflammatory mediators (IL-1β, TNF-α, inducible COX-2, CAMP) remained at much lower levels. Administration of a selective LPAR2 agonist DBIBB (1, 10 mg/kg, i.g., twice at 24 h and 30 min before IND treatment) dose-dependently reduced mucosal injury and neutrophil activation in enteropathy, but it also enhanced IND-induced elevation of several proinflammatory chemokines and cytokines. By assessing caspase-3 activation, we found significantly increased intestinal apoptosis in IND-treated Lpar2 −/− mice, but it was attenuated after DBIBB administration, especially in non-obese diabetic/severe combined immunodeficiency (NOD/SCID) mice. Finally, we showed that IND treatment reduced the plasma activity and expression of autotaxin (ATX), the main LPA-producing enzyme, and also reduced the intestinal expression of Lpar2 mRNA, which preceded the development of mucosal damage. We conclude that LPAR2 has a dual role in NSAID enteropathy, as it contributes to the maintenance of mucosal integrity after NSAID exposure, but also orchestrates the inflammatory responses associated with ulceration. Our study suggests that IND-induced inhibition of the ATX-LPAR2 axis is an early event in the pathogenesis of enteropathy.},
	year = {2024},
	eissn = {1745-7254},
	pages = {339-353},
	orcid-numbers = {Hutka, Barbara/0000-0002-7692-2744; László, Szilvia Bianka/0000-0001-9755-8972; Tóth, András Sebestyén/0000-0003-1761-1951; Paku, Sándor/0000-0003-2664-7729; Vörös, Imre/0000-0001-5922-6109; Pós, Zoltán/0000-0002-2574-7616; Varga, Zoltán/0000-0002-2758-0784; Balogh, Andrea/0000-0002-3007-0793; Benyó, Zoltán/0000-0001-6015-0359; Tigyi, Gabor/0000-0001-5371-171X; Gyires, Klára/0000-0002-4718-2345; Zádori, Zoltán Sándor/0000-0001-7312-618X}
}

@article{MTMT:34444783,
	title = {Depletion of muscularis macrophages ameliorates inflammation-driven dysmotility in murine colitis model},
	url = {https://m2.mtmt.hu/api/publication/34444783},
	author = {Ferenczi, Szilamér and Mógor, Fruzsina and Takács, Péter and Kovács, Tamás and Tóth, Viktória and Varga, Zoltán and Kovács, Krisztina and Lohinai, Zoltán and Vass, Koppány Csaba and Nagy, Nándor and Dóra, Dávid},
	doi = {10.1038/s41598-023-50059-7},
	journal-iso = {SCI REP},
	journal = {SCIENTIFIC REPORTS},
	volume = {13},
	unique-id = {34444783},
	issn = {2045-2322},
	abstract = {Previously, the presence of a blood-myenteric plexus barrier and its disruption was reported in experimentally induced colitis via a macrophage-dependent process. The aim of this study is to reveal how myenteric barrier disruption and subsequent neuronal injury affects gut motility in vivo in a murine colitis model. We induced colitis with dextran sulfate sodium (DSS), with the co-administration of liposome-encapsulated clodronate ( l -clodronate) to simultaneously deplete blood monocytes contributing to macrophage infiltration in the inflamed muscularis of experimental mice. DSS-treated animals receiving concurrent l -clodronate injection showed significantly decreased blood monocyte numbers and colon muscularis macrophage (MM) density compared to DSS-treated control (DSS-vehicle). DSS-clodronate-treated mice exhibited significantly slower whole gut transit time than DSS-vehicle-treated animals and comparable to that of controls. Experiments with oral gavage-fed Evans-blue dye showed similar whole gut transit times in DSS-clodronate-treated mice as in control animals. Furthermore, qPCR-analysis and immunofluorescence on colon muscularis samples revealed that factors associated with neuroinflammation and neurodegeneration, including Bax1, Hdac4, IL-18, Casp8 and Hif1a are overexpressed after DSS-treatment, but not in the case of concurrent l -clodronate administration. Our findings highlight that MM-infiltration in the muscularis layer is responsible for colitis-associated dysmotility and enteric neuronal dysfunction along with the release of mediators associated with neurodegeneration in a murine experimental model.},
	year = {2023},
	eissn = {2045-2322},
	orcid-numbers = {Kovács, Tamás/0000-0003-4127-4545; Tóth, Viktória/0000-0002-0426-2425; Varga, Zoltán/0000-0002-2758-0784; Lohinai, Zoltán/0000-0002-6442-9530; Nagy, Nándor/0000-0002-6223-5214}
}

@article{MTMT:34231258,
	title = {Cardioprotective MicroRNAs (ProtectomiRs) as potential novel cardioprotective therapeutics for acute myocardial infarction},
	url = {https://m2.mtmt.hu/api/publication/34231258},
	author = {Wiederanders, P. L. and Nagy, R. N. and Makkos, A. and Baranyai, T. and Giricz, Zoltán and Kiss, B. and Puskas, L. G. and Faragó, Nóra and Schulz, R. and Gyoengyoesi, M. and Varga, Zoltán and Görbe, Anikó and Ferdinandy, Péter},
	journal-iso = {N-S ARCH PHARMACOL},
	journal = {NAUNYN-SCHMIEDEBERGS ARCHIVES OF PHARMACOLOGY},
	volume = {396},
	unique-id = {34231258},
	issn = {0028-1298},
	year = {2023},
	eissn = {1432-1912},
	pages = {S23-S23},
	orcid-numbers = {Giricz, Zoltán/0000-0003-2036-8665; Varga, Zoltán/0000-0002-2758-0784; Görbe, Anikó/0000-0003-4908-1094; Ferdinandy, Péter/0000-0002-6424-6806}
}

@CONFERENCE{MTMT:34152489,
	title = {PHARMACOKINETIC CHARACTERISTICS OF A MICRORNA MIMIC AFTER INTRAVENOUS INJECTION IN MICE},
	url = {https://m2.mtmt.hu/api/publication/34152489},
	author = {Vörös, Imre and Makkos, András and Brenner, Gábor G and Ágg, Bence and Bencsik, Péter and Varga, Zoltán and Görbe, Anikó and Ferdinandy, Péter},
	booktitle = {FAMÉ 2023},
	unique-id = {34152489},
	year = {2023},
	pages = {258-258},
	orcid-numbers = {Bencsik, Péter/0000-0003-1936-6232; Varga, Zoltán/0000-0002-2758-0784; Görbe, Anikó/0000-0003-4908-1094; Ferdinandy, Péter/0000-0002-6424-6806}
}

@CONFERENCE{MTMT:34152487,
	title = {TRANSCRIPTOMIC PROFILING OF THE ADRENAL GLAND IN A TRANSLATIONAL RAT MODEL OF POSTINFARCTION HEART FAILURE},
	url = {https://m2.mtmt.hu/api/publication/34152487},
	author = {Váradi, Barnabás and Tóth, Viktória E. and Brenner, Gábor B. and Makkos, András and Onódi, Zsófia and Kucsera, Dániel and Vörös, Imre and Novák, Julianna and Sayour, Nabil Viktor and Ferdinandy, Péter and Varga, Zoltán},
	booktitle = {FAMÉ 2023},
	unique-id = {34152487},
	year = {2023},
	pages = {254-254},
	orcid-numbers = {Onódi, Zsófia/0000-0002-3746-8016; Ferdinandy, Péter/0000-0002-6424-6806; Varga, Zoltán/0000-0002-2758-0784}
}

@CONFERENCE{MTMT:34152485,
	title = {EFFECTS OF BLUNTING ANNEXIN A1 EXPRESION IN SMALL CELL LUNG CANCER CELL LINES},
	url = {https://m2.mtmt.hu/api/publication/34152485},
	author = {Paál, Ágnes and Takács, Ákos and Varga, Zoltán and Peták, István and Görbe, Anikó and Ferdinandy, Péter and Dóra, Dávid},
	booktitle = {FAMÉ 2023},
	unique-id = {34152485},
	year = {2023},
	pages = {241-241},
	orcid-numbers = {Varga, Zoltán/0000-0002-2758-0784; Peták, István/0000-0003-0422-9286; Görbe, Anikó/0000-0003-4908-1094; Ferdinandy, Péter/0000-0002-6424-6806}
}