@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:34729965,
	title = {IGF1R deficiency in vascular smooth muscle cells impairs myogenic autoregulation and cognition in mice},
	url = {https://m2.mtmt.hu/api/publication/34729965},
	author = {Miller, L.R. and Bickel, M.A. and Tarantini, S. and Runion, M.E. and Matacchiera, Z. and Vance, M.L. and Hibbs, C. and Vaden, H. and Nagykaldi, D. and Martin, T. and Bullen, E.C. and Pinckard, J. and Kiss, Tamás and Howard, E.W. and Yabluchanskiy, A. and Conley, S.M.},
	doi = {10.3389/fnagi.2024.1320808},
	journal-iso = {FRONT AGING NEUROSCI},
	journal = {FRONTIERS IN AGING NEUROSCIENCE},
	volume = {16},
	unique-id = {34729965},
	issn = {1663-4365},
	year = {2024},
	eissn = {1663-4365},
	orcid-numbers = {Kiss, Tamás/0000-0001-5339-5227}
}

@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:34391939,
	title = {Whole brain irradiation–induced endothelial dysfunction in the mouse brain},
	url = {https://m2.mtmt.hu/api/publication/34391939},
	author = {Kiss, Tamás and Ungvári, Anna Sára and Gulej, R. and Nyúl-Tóth, Ádám and Tarantini, Stefano and Benyó, Zoltán and Csik, B. and Yabluchanskiy, A. and Mukli, Péter and Csiszar, Anna and Ungvári, Zoltán István},
	doi = {10.1007/s11357-023-00990-4},
	journal-iso = {GEROSCIENCE},
	journal = {GEROSCIENCE: OFFICIAL JOURNAL OF THE AMERICAN AGING ASSOCIATION (AGE)},
	volume = {46},
	unique-id = {34391939},
	issn = {2509-2715},
	year = {2024},
	eissn = {2509-2723},
	pages = {531-541},
	orcid-numbers = {Kiss, Tamás/0000-0001-5339-5227; Tarantini, Stefano/0000-0001-5627-1430; Benyó, Zoltán/0000-0001-6015-0359; Mukli, Péter/0000-0003-4355-8103; Ungvári, Zoltán István/0000-0002-6035-6039}
}

@article{MTMT:34376788,
	title = {A role for the cystathionine-β-synthase /H2S axis in astrocyte dysfunction in the aging brain},
	url = {https://m2.mtmt.hu/api/publication/34376788},
	author = {Dey, A. and Pramanik, P.K. and Dwivedi, S.K.D. and Neizer-Ashun, F. and Kiss, Tamás and Ganguly, A. and Rice, H. and Mukherjee, P. and Xu, C. and Ahmad, M. and Csiszar, A. and Bhattacharya, R.},
	doi = {10.1016/j.redox.2023.102958},
	journal-iso = {REDOX BIOL},
	journal = {REDOX BIOLOGY},
	volume = {68},
	unique-id = {34376788},
	issn = {2213-2317},
	year = {2023},
	eissn = {2213-2317},
	orcid-numbers = {Kiss, Tamás/0000-0001-5339-5227}
}

@misc{MTMT:34182574,
	title = {IN CHILDREN LOW BIRTH WEIGHT MAY CONTRIBUTE TO THE DEVELOPMENT OF SEVERE COVID-19},
	url = {https://m2.mtmt.hu/api/publication/34182574},
	author = {Csizek, Zsófia and Matyas, Bukva and Cintia, Petes and Szabó, Attila and Kiss, Tamás},
	unique-id = {34182574},
	year = {2023},
	orcid-numbers = {Szabó, Attila/0000-0001-7321-9861; Kiss, Tamás/0000-0001-5339-5227}
}

@article{MTMT:34119854,
	title = {Elimination of senescent cells by treatment with Navitoclax/ABT263 reverses whole brain irradiation-induced blood-brain barrier disruption in the mouse brain},
	url = {https://m2.mtmt.hu/api/publication/34119854},
	author = {Gulej, Rafal and Nyúl-Tóth, Ádám and Ahire, Chetan and DelFavero, Jordan and Balasubramanian, Priya and Kiss, Tamás and Tarantini, Stefano and Benyó, Zoltán and Pacher, Pál and Csik, Boglarka and Yabluchanskiy, Andriy and Mukli, Péter and Kuan-Celarier, Anna and Krizbai, István Adorján and Campisi, Judith and Sonntag, William E. and Csiszar, Anna and Ungvári, Zoltán István},
	doi = {10.1007/s11357-023-00870-x},
	journal-iso = {GEROSCIENCE},
	journal = {GEROSCIENCE: OFFICIAL JOURNAL OF THE AMERICAN AGING ASSOCIATION (AGE)},
	volume = {45},
	unique-id = {34119854},
	issn = {2509-2715},
	year = {2023},
	eissn = {2509-2723},
	pages = {2983-3002},
	orcid-numbers = {Kiss, Tamás/0000-0001-5339-5227; Tarantini, Stefano/0000-0001-5627-1430; Benyó, Zoltán/0000-0001-6015-0359; Pacher, Pál/0000-0001-7036-8108; Mukli, Péter/0000-0003-4355-8103; Ungvári, Zoltán István/0000-0002-6035-6039}
}

@article{MTMT:34093747,
	title = {Galectin-1 as a marker for microglia activation in the aging brain},
	url = {https://m2.mtmt.hu/api/publication/34093747},
	author = {Kiss, Tamás and Mir, Mohd Yaqub and Stefancsik, Gergely and Ganbat, Gantulga and Askarova, Aruzhan and Monostori, Éva and Dulka, Karolina and Szebeni, Gábor and Nyúl-Tóth, Ádám and Csiszar, Anna and Légrádi, Ádám},
	doi = {10.1016/j.brainres.2023.148517},
	journal-iso = {BRAIN RES},
	journal = {BRAIN RESEARCH},
	volume = {1818},
	unique-id = {34093747},
	issn = {0006-8993},
	abstract = {Microglia cells, the immune cells residing in the brain, express immune regulatory molecules that have a central role in the manifestation of age-related brain characteristics. Our hypothesis suggests that galectin-1, an anti-inflammatory member of the beta-galactoside-binding lectin family, regulates microglia and neuroinflammation in the aging brain. Through our in-silico analysis, we discovered a subcluster of microglia in the aged mouse brain that exhibited increased expression of galectin-1 mRNA. In our Western blotting experiments, we observed a decrease in galectin-1 protein content in our rat primary cortical cultures over time. Additionally, we found that the presence of lipopolysaccharide, an immune activator, significantly increased the expression of galectin-1 protein in microglial cells. Utilizing flow cytometry, we determined that a portion of the galectin-1 protein was localized on the surface of the microglial cells. As cultivation time increased, we observed a decrease in the expression of activation-coupled molecules in microglial cells, indicating cellular exhaustion. In our mixed rat primary cortical cell cultures, we noted a transition of amoeboid microglial cells labeled with OX42(CD11b/c) to a ramified, branched phenotype during extended cultivation, accompanied by a complete disappearance of galectin-1 expression. By analyzing the transcriptome of a distinct microglial subpopulation in an animal model of aging, we established a correlation between chronological aging and galectin-1 expression. Furthermore, our in vitro study demonstrated that galectin-1 expression is associated with the functional activation state of microglial cells exhibiting specific amoeboid morphological characteristics. Based on our findings, we identify galectin-1 as a marker for microglia activation in the context of aging.},
	keywords = {Aging; Galectin-1; neuroinflammation; microglia},
	year = {2023},
	eissn = {1872-6240},
	orcid-numbers = {Kiss, Tamás/0000-0001-5339-5227; Stefancsik, Gergely/0000-0002-2098-652X; Monostori, Éva/0000-0002-7442-3562; Dulka, Karolina/0000-0002-7368-8198; Szebeni, Gábor/0000-0002-6998-5632; Légrádi, Ádám/0000-0001-7994-1935}
}

@article{MTMT:33989450,
	title = {Accelerated cerebromicrovascular senescence contributes to cognitive decline in a mouse model of paclitaxel (Taxol)-induced chemobrain},
	url = {https://m2.mtmt.hu/api/publication/33989450},
	author = {Ahire, Chetan and Nyúl-Tóth, Ádám and DelFavero, Jordan and Gulej, Rafal and Faakye, Janet A. and Tarantini, Stefano and Kiss, Tamás and Kuan-Celarier, Anna and Balasubramanian, Priya and Ungvári, Anna Sára and Tarantini, Amber and Nagaraja, Raghavendra and Yan, Feng and Tang, Qinggong and Mukli, Péter and Csípő, Tamás and Yabluchanskiy, Andriy and Campisi, Judith and Ungvári, Zoltán István and Csiszar, Anna},
	doi = {10.1111/acel.13832},
	journal-iso = {AGING CELL},
	journal = {AGING CELL},
	volume = {22},
	unique-id = {33989450},
	issn = {1474-9718},
	abstract = {Chemotherapy-induced cognitive impairment ("chemobrain") is a frequent side-effect in cancer survivors treated with paclitaxel (PTX). The mechanisms responsible for PTX-induced cognitive impairment remain obscure, and there are no effective treatments or prevention strategies. Here, we test the hypothesis that PTX induces endothelial senescence, which impairs microvascular function and contributes to the genesis of cognitive decline. We treated transgenic p16-3MR mice, which allows the detection and selective elimination of senescent cells, with PTX (5 mg/kg/day, 2 cycles; 5 days/cycle). PTX-treated and control mice were tested for spatial memory performance, neurovascular coupling (NVC) responses (whisker-stimulation-induced increases in cerebral blood flow), microvascular density, blood-brain barrier (BBB) permeability and the presence of senescent endothelial cells (by flow cytometry and single-cell transcriptomics) at 6 months post-treatment. PTX induced senescence in endothelial cells, which associated with microvascular rarefaction, NVC dysfunction, BBB disruption, neuroinflammation, and impaired performance on cognitive tasks. To establish a causal relationship between PTX-induced senescence and impaired microvascular functions, senescent cells were depleted from PTX-treated animals (at 3 months post-treatment) by genetic (ganciclovir) or pharmacological (treatment with the senolytic drug ABT263/Navitoclax) means. In PTX treated mice, both treatments effectively eliminated senescent endothelial cells, rescued endothelium-mediated NVC responses and BBB integrity, increased capillarization and improved cognitive performance. Our findings suggest that senolytic treatments can be a promising strategy for preventing chemotherapy-induced cognitive impairment.},
	keywords = {DYSFUNCTION; INHIBITION; CANCER; CHEMOTHERAPY; CHEMOTHERAPY; DEMENTIA; ANGIOGENESIS; Aging; BLOOD-BRAIN-BARRIER; senescence; CELL BIOLOGY; cellular senescence; navitoclax; Functional hyperemia; BETA-AMYLOID GENERATION; Chemotherapy-induced cognitive impairment},
	year = {2023},
	eissn = {1474-9726},
	orcid-numbers = {Tarantini, Stefano/0000-0001-5627-1430; Kiss, Tamás/0000-0001-5339-5227; Mukli, Péter/0000-0003-4355-8103; Ungvári, Zoltán István/0000-0002-6035-6039}
}