@article{MTMT:34803971,
	title = {Predictive factors of basic palliative and hospice care among patients with cancer visiting the emergency department in a Hungarian tertiary care center},
	url = {https://m2.mtmt.hu/api/publication/34803971},
	author = {Varga, Csaba and Springó, Zsolt and Koch, M. and Prenek, L. and Porcsa, L. and Bellyei, Szabolcs and Rumi, L. and Szabó, É. and Ungvári, Zoltán István and Girán, K. and Kiss, I. and Pozsgai, É.},
	doi = {10.1016/j.heliyon.2024.e29348},
	journal-iso = {HELIYON},
	journal = {HELIYON},
	volume = {10},
	unique-id = {34803971},
	year = {2024},
	eissn = {2405-8440},
	orcid-numbers = {Ungvári, Zoltán István/0000-0002-6035-6039}
}

@article{MTMT:34773870,
	title = {Accelerated Aging Induced by an Unhealthy High-Fat Diet: Initial Evidence for the Role of Nrf2 Deficiency and Impaired Stress Resilience in Cellular Senescence},
	url = {https://m2.mtmt.hu/api/publication/34773870},
	author = {Balasubramanian, Priya and Kiss, Tamás and Gulej, Rafal and Nyúl-Tóth, Ádám and Tarantini, Stefano and Yabluchanskiy, Andriy and Ungvári, Zoltán István and Csiszar, Anna},
	doi = {10.3390/nu16070952},
	journal-iso = {NUTRIENTS},
	journal = {NUTRIENTS},
	volume = {16},
	unique-id = {34773870},
	abstract = {High-fat diets (HFDs) have pervaded modern dietary habits, characterized by their excessive saturated fat content and low nutritional value. Epidemiological studies have compellingly linked HFD consumption to obesity and the development of type 2 diabetes mellitus. Moreover, the synergistic interplay of HFD, obesity, and diabetes expedites the aging process and prematurely fosters age-related diseases. However, the underlying mechanisms driving these associations remain enigmatic. One of the most conspicuous hallmarks of aging is the accumulation of highly inflammatory senescent cells, with mounting evidence implicating increased cellular senescence in the pathogenesis of age-related diseases. Our hypothesis posits that HFD consumption amplifies senescence burden across multiple organs. To scrutinize this hypothesis, we subjected mice to a 6-month HFD regimen, assessing senescence biomarker expression in the liver, white adipose tissue, and the brain. Aging is intrinsically linked to impaired cellular stress resilience, driven by dysfunction in Nrf2-mediated cytoprotective pathways that safeguard cells against oxidative stress-induced senescence. To ascertain whether Nrf2-mediated pathways shield against senescence induction in response to HFD consumption, we explored senescence burden in a novel model of aging: Nrf2-deficient (Nrf2+/−) mice, emulating the aging phenotype. Our initial findings unveiled significant Nrf2 dysfunction in Nrf2+/− mice, mirroring aging-related alterations. HFD led to substantial obesity, hyperglycemia, and impaired insulin sensitivity in both Nrf2+/− and Nrf2+/+ mice. In control mice, HFD primarily heightened senescence burden in white adipose tissue, evidenced by increased Cdkn2a senescence biomarker expression. In Nrf2+/− mice, HFD elicited a significant surge in senescence burden across the liver, white adipose tissue, and the brain. We postulate that HFD-induced augmentation of senescence burden may be a pivotal contributor to accelerated organismal aging and the premature onset of age-related diseases.},
	year = {2024},
	eissn = {2072-6643},
	orcid-numbers = {Kiss, Tamás/0000-0001-5339-5227; Gulej, Rafal/0000-0002-9958-707X; Tarantini, Stefano/0000-0001-5627-1430; Ungvári, Zoltán István/0000-0002-6035-6039}
}

@article{MTMT:34760823,
	title = {Editorial: Endocrine regulation of aging: impacts of humoral factors and circulating mediators},
	url = {https://m2.mtmt.hu/api/publication/34760823},
	author = {Petersen, B. and Negri, S. and Milan, M. and Reyff, Z. and Ballard, C. and Ihuoma, J. and Ungvári, Zoltán István and Tarantini, Stefano},
	doi = {10.3389/fendo.2024.1387435},
	journal-iso = {FRONT ENDOCRINOL},
	journal = {FRONTIERS IN ENDOCRINOLOGY},
	volume = {15},
	unique-id = {34760823},
	issn = {1664-2392},
	year = {2024},
	eissn = {1664-2392},
	orcid-numbers = {Ungvári, Zoltán István/0000-0002-6035-6039; Tarantini, Stefano/0000-0001-5627-1430}
}

@article{MTMT:34756276,
	title = {Neurovascular coupling impairment as a mechanism for cognitive deficits in COVID-19},
	url = {https://m2.mtmt.hu/api/publication/34756276},
	author = {Owens, Cameron D and Bonin Pinto, Camila and Detwiler, Sam and Olay, Lauren and Pinaffi-Langley, Ana Clara da C and Mukli, Péter and Péterfi, Anna and Szarvas, Zsófia and James, Judith A and Galvan, Veronica and Tarantini, Stefano and Csiszar, Anna and Ungvári, Zoltán István and Kirkpatrick, Angelia C and Prodan, Calin I and Yabluchanskiy, Andriy},
	doi = {10.1093/braincomms/fcae080},
	journal-iso = {BRAIN COMMUN},
	journal = {BRAIN COMMUNICATIONS},
	volume = {6},
	unique-id = {34756276},
	abstract = {Components that comprise our brain parenchymal and cerebrovascular structures provide a homeostatic environment for proper neuronal function to ensure normal cognition. Cerebral insults (e.g. ischaemia, microbleeds and infection) alter cellular structures and physiologic processes within the neurovascular unit and contribute to cognitive dysfunction. COVID-19 has posed significant complications during acute and convalescent stages in multiple organ systems, including the brain. Cognitive impairment is a prevalent complication in COVID-19 patients, irrespective of severity of acute SARS-CoV-2 infection. Moreover, overwhelming evidence from in vitro, preclinical and clinical studies has reported SARS-CoV-2-induced pathologies in components of the neurovascular unit that are associated with cognitive impairment. Neurovascular unit disruption alters the neurovascular coupling response, a critical mechanism that regulates cerebromicrovascular blood flow to meet the energetic demands of locally active neurons. Normal cognitive processing is achieved through the neurovascular coupling response and involves the coordinated action of brain parenchymal cells (i.e. neurons and glia) and cerebrovascular cell types (i.e. endothelia, smooth muscle cells and pericytes). However, current work on COVID-19-induced cognitive impairment has yet to investigate disruption of neurovascular coupling as a causal factor. Hence, in this review, we aim to describe SARS-CoV-2's effects on the neurovascular unit and how they can impact neurovascular coupling and contribute to cognitive decline in acute and convalescent stages of the disease. Additionally, we explore potential therapeutic interventions to mitigate COVID-19-induced cognitive impairment. Given the great impact of cognitive impairment associated with COVID-19 on both individuals and public health, the necessity for a coordinated effort from fundamental scientific research to clinical application becomes imperative. This integrated endeavour is crucial for mitigating the cognitive deficits induced by COVID-19 and its subsequent burden in this especially vulnerable population.},
	year = {2024},
	eissn = {2632-1297},
	orcid-numbers = {Owens, Cameron D/0000-0002-5020-2810; Mukli, Péter/0000-0003-4355-8103; Szarvas, Zsófia/0000-0002-0022-5053; Tarantini, Stefano/0000-0001-5627-1430; Ungvári, Zoltán István/0000-0002-6035-6039; Yabluchanskiy, Andriy/0000-0002-9648-7161}
}

@article{MTMT:34724864,
	title = {Vascular smooth muscle cell-specific Igf1r deficiency exacerbates the development of hypertension-induced cerebral microhemorrhages and gait defects},
	url = {https://m2.mtmt.hu/api/publication/34724864},
	author = {Miller, L.R. and Bickel, M.A. and Vance, M.L. and Vaden, H. and Nagykaldi, D. and Nyúl-Tóth, Ádám and Bullen, E.C. and Gautam, T. and Tarantini, Stefano and Yabluchanskiy, A. and Kiss, Tamás and Ungvári, Zoltán István and Conley, S.M.},
	doi = {10.1007/s11357-024-01090-7},
	journal-iso = {GEROSCIENCE},
	journal = {GEROSCIENCE: OFFICIAL JOURNAL OF THE AMERICAN AGING ASSOCIATION (AGE)},
	volume = {46},
	unique-id = {34724864},
	issn = {2509-2715},
	year = {2024},
	eissn = {2509-2723},
	pages = {3481-3501},
	orcid-numbers = {Tarantini, Stefano/0000-0001-5627-1430; Kiss, Tamás/0000-0001-5339-5227; Ungvári, Zoltán István/0000-0002-6035-6039}
}

@article{MTMT:34500888,
	title = {Irradiation-induced hair graying in mice: an experimental model to evaluate the effectiveness of interventions targeting oxidative stress, DNA damage prevention, and cellular senescence},
	url = {https://m2.mtmt.hu/api/publication/34500888},
	author = {Ungvári, Anna Sára and Kiss, Tamás and Gulej, R. and Tarantini, Stefano and Csik, B. and Yabluchanskiy, A. and Mukli, Péter and Csiszar, Anna and Harris, M.L. and Ungvári, Zoltán István},
	doi = {10.1007/s11357-023-01042-7},
	journal-iso = {GEROSCIENCE},
	journal = {GEROSCIENCE: OFFICIAL JOURNAL OF THE AMERICAN AGING ASSOCIATION (AGE)},
	volume = {46},
	unique-id = {34500888},
	issn = {2509-2715},
	year = {2024},
	eissn = {2509-2723},
	pages = {3105-3122},
	orcid-numbers = {Kiss, Tamás/0000-0001-5339-5227; Tarantini, Stefano/0000-0001-5627-1430; Mukli, Péter/0000-0003-4355-8103; Ungvári, Zoltán István/0000-0002-6035-6039}
}

@article{MTMT:34482135,
	title = {NO Deficiency Compromises Inter- and Intrahemispheric Blood Flow Adaptation to Unilateral Carotid Artery Occlusion},
	url = {https://m2.mtmt.hu/api/publication/34482135},
	author = {Hricisák, László and Pál, Éva and Nagy, Dorina and Delank, Max and Polycarpou, Andreas and Fülöp, Ágnes and Sándor, Péter and Sótonyi, Péter and Ungvári, Zoltán István and Benyó, Zoltán},
	doi = {10.3390/ijms25020697},
	journal-iso = {INT J MOL SCI},
	journal = {INTERNATIONAL JOURNAL OF MOLECULAR SCIENCES},
	volume = {25},
	unique-id = {34482135},
	issn = {1661-6596},
	abstract = {Carotid artery stenosis (CAS) affects approximately 5–7.5% of older adults and is recognized as a significant risk factor for vascular cognitive impairment (VCI). The impact of CAS on cerebral blood flow (CBF) within the ipsilateral hemisphere relies on the adaptive capabilities of the cerebral microcirculation. In this study, we aimed to test the hypothesis that the impaired availability of nitric oxide (NO) compromises CBF homeostasis after unilateral carotid artery occlusion (CAO). To investigate this, three mouse models exhibiting compromised production of NO were tested: NOS1 knockout, NOS1/3 double knockout, and mice treated with the NO synthesis inhibitor L-NAME. Regional CBF changes following CAO were evaluated using laser-speckle contrast imaging (LSCI). Our findings demonstrated that NOS1 knockout, NOS1/3 double knockout, and L-NAME-treated mice exhibited impaired CBF adaptation to CAO. Furthermore, genetic deficiency of one or two NO synthase isoforms increased the tortuosity of pial collaterals connecting the frontoparietal and temporal regions. In conclusion, our study highlights the significant contribution of NO production to the functional adaptation of cerebrocortical microcirculation to unilateral CAO. We propose that impaired bioavailability of NO contributes to the impaired CBF homeostasis by altering inter- and intrahemispheric blood flow redistribution after unilateral disruption of carotid artery flow.},
	year = {2024},
	eissn = {1422-0067},
	orcid-numbers = {Hricisák, László/0000-0001-8320-2166; Pál, Éva/0000-0003-1793-1912; Nagy, Dorina/0000-0003-2067-753X; Fülöp, Ágnes/0000-0001-8132-2084; Sándor, Péter/0000-0002-1257-8235; Sótonyi, Péter/0000-0002-2216-4298; Ungvári, Zoltán István/0000-0002-6035-6039; Benyó, Zoltán/0000-0001-6015-0359}
}

@article{MTMT:34477401,
	title = {Impaired Neurovascular Coupling and Increased Functional Connectivity in the Frontal Cortex Predict Age-Related Cognitive Dysfunction},
	url = {https://m2.mtmt.hu/api/publication/34477401},
	author = {Mukli, Péter and Pinto, Camila B and Owens, Cameron D and Csípő, Tamás and Lipécz, Ágnes and Szarvas, Zsófia and Péterfi, Anna and Langley, Ana Clara da Costa Pinaffi and Hoffmeister, Jordan and Rácz, Frigyes Sámuel and Perry, Jonathan W and Tarantini, Stefano and Nyúl-Tóth, Ádám and Sorond, Farzaneh A and Yang, Yuan and James, Judith A and Kirkpatrick, Angelia C and Prodan, Calin I and Tóth, Péter József and Galindo, Juliette and Gardner, Andrew W and Sonntag, William E and Csiszar, Anna and Ungvári, Zoltán István and Yabluchanskiy, Andriy},
	doi = {10.1002/advs.202303516},
	journal-iso = {ADV SCI},
	journal = {ADVANCED SCIENCE},
	volume = {11},
	unique-id = {34477401},
	abstract = {Impaired cerebrovascular function contributes to the genesis of age-related cognitive decline. In this study, the hypothesis is tested that impairments in neurovascular coupling (NVC) responses and brain network function predict cognitive dysfunction in older adults. Cerebromicrovascular and working memory function of healthy young (n = 21, 33.2±7.0 years) and aged (n = 30, 75.9±6.9 years) participants are assessed. To determine NVC responses and functional connectivity (FC) during a working memory (n-back) paradigm, oxy- and deoxyhemoglobin concentration changes from the frontal cortex using functional near-infrared spectroscopy are recorded. NVC responses are significantly impaired during the 2-back task in aged participants, while the frontal networks are characterized by higher local and global connection strength, and dynamic FC (p < 0.05). Both impaired NVC and increased FC correlate with age-related decline in accuracy during the 2-back task. These findings suggest that task-related brain states in older adults require stronger functional connections to compensate for the attenuated NVC responses associated with working memory load.},
	keywords = {Aging; cognitive decline; functional connectivity; Neurovascular coupling; functional near-infrared spectroscopy},
	year = {2024},
	eissn = {2198-3844},
	orcid-numbers = {Mukli, Péter/0000-0003-4355-8103; Szarvas, Zsófia/0000-0002-0022-5053; Rácz, Frigyes Sámuel/0000-0001-9077-498X; Tarantini, Stefano/0000-0001-5627-1430; Ungvári, Zoltán István/0000-0002-6035-6039}
}

@article{MTMT:34474845,
	title = {Rejuvenation of cerebromicrovascular function in aged mice through heterochronic parabiosis: insights into neurovascular coupling and the impact of young blood factors},
	url = {https://m2.mtmt.hu/api/publication/34474845},
	author = {Gulej, R. and Nyúl-Tóth, Ádám and Csik, B. and Petersen, B. and Faakye, J. and Negri, S. and Chandragiri, S.S. and Mukli, Péter and Yabluchanskiy, A. and Conley, S. and Huffman, D.M. and Csiszar, Anna and Tarantini, Stefano and Ungvári, Zoltán István},
	doi = {10.1007/s11357-023-01039-2},
	journal-iso = {GEROSCIENCE},
	journal = {GEROSCIENCE: OFFICIAL JOURNAL OF THE AMERICAN AGING ASSOCIATION (AGE)},
	volume = {46},
	unique-id = {34474845},
	issn = {2509-2715},
	year = {2024},
	eissn = {2509-2723},
	pages = {327-347},
	orcid-numbers = {Mukli, Péter/0000-0003-4355-8103; Tarantini, Stefano/0000-0001-5627-1430; Ungvári, Zoltán István/0000-0002-6035-6039}
}

@article{MTMT:34452959,
	title = {PCSK9: an emerging player in cardiometabolic aging and its potential as a therapeutic target and biomarker},
	url = {https://m2.mtmt.hu/api/publication/34452959},
	author = {Csiszar, Anna and Tarantini, Stefano and Yabluchanskiy, A. and Ungvári, Zoltán István},
	doi = {10.1007/s11357-023-01003-0},
	journal-iso = {GEROSCIENCE},
	journal = {GEROSCIENCE: OFFICIAL JOURNAL OF THE AMERICAN AGING ASSOCIATION (AGE)},
	volume = {46},
	unique-id = {34452959},
	issn = {2509-2715},
	year = {2024},
	eissn = {2509-2723},
	pages = {257-263},
	orcid-numbers = {Tarantini, Stefano/0000-0001-5627-1430; Ungvári, Zoltán István/0000-0002-6035-6039}
}