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001-es BibID:	BIBFORM082129
035-os BibID:	(WOS)000493693900001 (Scopus)85074812973
Első szerző:	Tarantini, Stefano
Cím:	Treatment with the poly(ADP-ribose) polymerase inhibitor PJ-34 improves cerebromicrovascular endothelial function, neurovascular coupling responses and cognitive performance in aged mice, supporting the NAD+ depletion hypothesis of neurovascular aging / Tarantini Stefano, Yabluchanskiy Andriy, Csipo Tamas, Fulop Gabor, Kiss Tamas, Balasubramanian Priya, DelFavero Jordan, Ahire Chetan, Ungvari Anna, Nyúl-Tóth Ádám, Farkas Eszter, Benyo Zoltan, Tóth Attila, Csiszar Anna, Ungvari Zoltan
Dátum:	2019
ISSN:	2509-2715 2509-2723
Megjegyzések:	Adjustment of cerebral blood flow (CBF) to neuronal activity via neurovascular coupling (NVC) plays an important role in the maintenance of healthy cognitive function. Strong evidence demonstrates that age-related cerebromicrovascular endothelial dysfunction and consequential impairment of NVC responses contribute importantly to cognitive decline. Recent studies demonstrate that NAD(+) availability decreases with age in the vasculature and that supplemental NAD(+) precursors can ameliorate cerebrovascular dysfunction, rescuing NVC responses and improving cognitive performance in aged mice. The mechanisms underlying the age-related decline in [NAD(+)] in cells of the neurovascular unit are likely multifaceted and may include increased utilization of NAD(+) by activated poly (ADP-ribose) polymerase (PARP-1). The present study was designed to test the hypothesis that inhibition of PARP-1 activity may confer protective effects on neurovascular function in aging, similar to the recently demonstrated protective effects of treatment with the NAD+ precursor nicotinamide mononucleotide (NMN). To test this hypothesis, 24-month-old C57BL/6 mice were treated with PJ-34, a potent PARP inhibitor, for 2 weeks. NVC was assessed by measuring CBF responses (laser speckle contrast imaging) in the somatosensory whisker barrel cortex evoked by contralateral whisker stimulation. We found that NVC responses were significantly impaired in aged mice. Treatment with PJ-34 improved NVC responses by increasing endothelial NO-mediated vasodilation, which was associated with significantly improved spatial working memory. PJ-34 treatment also improved endothelium-dependent acetylcholine-induced relaxation of aorta rings. Thus, PARP-1 activation, likely by decreasing NAD(+) availability, contributes to age-related endothelial dysfunction and neurovascular uncoupling, exacerbating cognitive decline. The cerebromicrovascular protective effects of pharmacological inhibition of PARP-1 highlight the preventive and therapeutic potential of treatments that restore NAD+ homeostasis as effective interventions in patients at risk for vascular cognitive impairment (VCI).
Tárgyszavak:	Orvostudományok Elméleti orvostudományok idegen nyelvű folyóiratközlemény külföldi lapban folyóiratcikk Cellular energetics Oxidative stress ROS Endothelial dysfunction Functional hyperemia Microcirculation Senescence
Megjelenés:	GeroScience. - 41 : 5 (2019), p. 533-542. -
További szerzők:	Yabluchanskiy, Andriy Csípő Tamás (1990-) Fülöp Gábor Áron (1988-) (általános orvos) Kiss Tamás Balasubramanian, Priya DelFavero, Jordan Ahire, Chetan Ungvári Anna Nyúl-Tóth Ádám Farkas Eszter Benyó Zoltán Tóth Attila (1971-) (biológus) Csiszár Anna Ungvári Zoltán
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001-es BibID:	BIBFORM117425
035-os BibID:	(Scopus)85179338215 (WoS)001115572500001
Első szerző:	Ungvári Zoltán
Cím:	The Semmelweis Study : a longitudinal occupational cohort study within the framework of the Semmelweis Caring University Model Program for supporting healthy aging / Zoltan Ungvari, Adam G. Tabák, Roza Adany, György Purebl, Csilla Kaposvári, Vince Fazekas-Pongor, Tamás Csípő, Zsófa Szarvas, Krisztián Horváth, Peter Mukli, Piroska Balog, Robert Bodizs, Peter Ujma, Adrienne Stauder, Daniel W. Belsky, Illés Kovács, Andriy Yabluchanskiy, Andrea B. Maier, Mariann Moizs, Piroska Östlin, Yongjie Yon, Péter Varga, Zoltán Vokó, Magor Papp, István Takács, Barna Vásárhelyi, Péter Torzsa, Péter Ferdinandy, Anna Csiszar, Zoltán Benyó, Attila J. Szabó, Gabriella Dörnyei, Mika Kivimäki, Miklos Kellermayer, Bela Merkely
Dátum:	2024
ISSN:	2509-2715 2509-2723
Megjegyzések:	The Semmelweis Study is a prospective occupational cohort study that seeks to enroll all employees of Semmelweis University (Budapest, Hungary) aged 25 years and older, with a population of 8866 people, 70.5% of whom are women. The study builds on the successful experiences of the Whitehall II study and aims to investigate the complex relationships between lifestyle, environmental, and occupational risk factors, and the development and progression of chronic age-associated diseases. An important goal of the Semmelweis Study is to identify groups of people who are aging unsuccessfully and therefore have an increased risk of developing age-associated diseases. To achieve this, the study takes a multidisciplinary approach, collecting economic, social, psychological, cognitive, health, and biological data. The Semmelweis Study comprises a baseline data collection with open healthcare data linkage, followed by repeated data collection waves every 5 years. Data are collected through computer-assisted self-completed questionnaires, followed by a physical health examination, physiological measurements, and the assessment of biomarkers. This article provides a comprehensive overview of the Semmelweis Study, including its origin, context, objectives, design, relevance, and expected contributions.
Tárgyszavak:	Orvostudományok Egészségtudományok idegen nyelvű folyóiratközlemény külföldi lapban folyóiratcikk Age-associated diseases Biological age Central Europe Epidemiology Health Promoting University Healthy aging Workplace cohort
Megjelenés:	GeroScience. - 46 : 1 (2024), p. 191-218. -
További szerzők:	Tabák Ádám G. Ádány Róza (1952-) (megelőző orvostan és népegészségtan szakorvos) Purebl György Kaposvári Csilla Fazekas-Pongor Vince Csípő Tamás (1990-) Szarvas Zsófia Horváth Krisztián Mukli Péter Balog Róbert Bódizs Róbert Ujma Péter Stauder Adrienne Belsky, Daniel W. Kovács Illés Yabluchanskiy, Andriy Maier, Andrea B. Moizs Marianna (1964-) (orvos) Östlin Piroska Yon, Yongjie Varga Péter Vokó Zoltán (1968-) (epidemiológus) Papp Magor Csongor (1978-) (háziorvostan szakorvos) Takács István Vásárhelyi Barna Torzsa Péter Ferdinándy Péter Csiszár Anna Benyó Zoltán Szabó Attila (gyermekgyógyász Budapest) Dörnyei Gabriella Kivimäki, Mika Kellermayer Miklós Merkely Béla (1965-) (orvos)
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001-es BibID:	BIBFORM099946
035-os BibID:	(WOS)000492656400001 (Scopus)85074498620
Első szerző:	Ungvári Zoltán
Cím:	Nrf2 dysfunction and impaired cellular resilience to oxidative stressors in the aged vasculature : from increased cellular senescence to the pathogenesis of age-related vascular diseases / Ungvari Zoltan, Tarantini Stefano, Nyúl-Tóth Ádám, Kiss Tamas, Yabluchanskiy Andriy, Csipo Tamas, Balasubramanian Priya, Lipecz Agnes, Benyo Zoltan, Csiszar Anna
Dátum:	2019
ISSN:	2509-2715 2509-2723
Megjegyzések:	Aging is associated with increased oxidative stress in vascular endothelial and smooth muscle cells, which contribute to the development of a wide range of diseases affecting the circulatory system in older adults. There is growing evidence that in addition to increased production of reactive oxygen species (ROS), aging critically impairs pathways determining cellular resilience to oxidative stressors. In young organisms, the evolutionarily conserved nuclear factor-erythroid-2-related factor 2 (Nrf2)-mediated antioxidant response pathway maintains cellular reduction-oxidation homeostasis and promotes a youthful cellular phenotype by regulating the transcription of an array of cytoprotective (antioxidant, pro-survival, anti-inflammatory and macromolecular damage repair) genes. A critical mechanism by which increased ROS production and Nrf2 dysfunction promote vascular aging and exacerbate pathogenesis of age-related vascular diseases is induction of cellular senescence, an evolutionarily conserved cellular stress response mechanism. Senescent cells cease dividing and undergo distinctive phenotypic alterations, contributing to impairment of angiogenic processes, chronic sterile inflammation, remodeling of the extracellular matrix, and barrier dysfunction. Herein, we review mechanisms contributing to dysregulation of Nrf2-driven cytoprotective responses in the aged vasculature and discuss the multifaceted role of Nrf2 dysfunction in the genesis of age-related pathologies affecting the circulatory system, including its role in induction of cellular senescence. Therapeutic strategies that restore Nrf2 signaling and improve vascular resilience in aging are explored to reduce cardiovascular mortality and morbidity in older adults.
Tárgyszavak:	Orvostudományok Elméleti orvostudományok idegen nyelvű folyóiratközlemény külföldi lapban folyóiratcikk Antioxidant Atherosclerosis Nrf2 deficiency Nrf2 dysfunction Oxidative stress Reactive oxygen species Senescence Stress resistance Vascular aging Vascular cognitive impairment
Megjelenés:	GeroScience. - 41 : 6 (2019), p. 727-738. -
További szerzők:	Tarantini, Stefano Nyúl-Tóth Ádám Kiss Tamás (1950-) (vegyész) Yabluchanskiy, Andriy Csípő Tamás (1990-) Balasubramanian, Priya Lipécz Ágnes Benyó Zoltán Csiszár Anna
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