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001-es BibID:	BIBFORM100041
035-os BibID:	(WOS)000739793800001 (Scopus)85122483976
Első szerző:	Nyúl-Tóth Ádám
Cím:	Cerebral venous congestion exacerbates cerebral microhemorrhages in mice / Nyul-Toth Adam, Fulop Gabor A., Tarantini Stefano, Kiss Tamas, Ahire Chetan, Faakye Janet A., Ungvari Anna, Toth Peter, Toth Attila, Csiszar Anna, Ungvari Zoltan
Dátum:	2022
ISSN:	2509-2715 2509-2723
Megjegyzések:	Cerebral microhemorrhages (CMHs; microbleeds), which are small focal intracerebral hemorrhages, importantly contribute to the pathogenesis of cognitive decline and dementia in older adults. Although recently it has been increasingly recognized that the venous side of the cerebral circulation likely plays a fundamental role in the pathogenesis of a wide spectrum of cerebrovascular and brain disorders, its role in the pathogenesis of CMHs has never been studied. The present study was designed to experimentally test the hypothesis that venous congestion can exacerbate the genesis of CMHs. Increased cerebral venous pressure was induced by internal and external jugular vein ligation (JVL) in C57BL/6 mice in which systemic hypertension was induced by treatment with angiotensin II plus L-NAME. Histological analysis (diaminobenzidine staining) showed that mice with JVL developed multiple CMHs. CMHs in mice with JVL were often localized adjacent to veins and venules and their morphology was consistent with venous origin of the bleeds. In brains of mice with JVL, a higher total count of CMHs was observed compared to control mice. CMHs were distributed widely in the brain of mice with JVL, including the cortical gray matter, brain stem, the basal ganglia, subcortical white matter, cerebellum, and the hippocampi. In mice with JVL, there were more CMHs predominantly in cerebral cortex, brain stem, and cerebellum than in control mice. CMH burden, defined as total CMH volume, also significantly increased in mice with JVL. Thus, cerebral venous congestion can exacerbate CMHs. These observations have relevance to the pathogenesis of cognitive impairment associated with right heart failure as well as elevated cerebral venous pressure due to jugular venous reflux in older adults.
Tárgyszavak:	Orvostudományok Elméleti orvostudományok idegen nyelvű folyóiratközlemény külföldi lapban folyóiratcikk Microbleed Vascular contributions to cognitive impairment and dementia (VCID) VCI Vein Venous congestion Heart failure Cerebral circulation ICH Vascular cognitive impairment Intracerebral hemorrhage
Megjelenés:	GeroScience. - 44 : 2 (2022), p. 805-816. -
További szerzők:	Fülöp Gábor Áron (1988-) (általános orvos) Tarantini, Stefano Kiss Tamás Ahire, Chetan Faakye, Janet A. Ungvári Anna Tóth Péter Tóth Attila (1971-) (biológus) Csiszár Anna Ungvári Zoltán
Pályázati támogatás:	TKP2020-IKA-04 Egyéb
Internet cím:	Szerző által megadott URL DOI Intézményi repozitóriumban (DEA) tárolt változat
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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
Internet cím:	Szerző által megadott URL DOI Intézményi repozitóriumban (DEA) tárolt változat
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001-es BibID:	BIBFORM126488
035-os BibID:	(scopus)85214130499 (wos)001389612700001
Első szerző:	Ungvári Anna
Cím:	Sex-specific mechanisms in vascular aging : exploring cellular and molecular pathways in the pathogenesis of age-related cardiovascular and cerebrovascular diseases / Ungvari Anna, Gulej Rafal, Patai Roland, Papp Zoltan, Toth Attila, Szabó Attila Á., Podesser Bruno K., Sótonyi Péter, Benyó Zoltán, Yabluchanskiy Andriy, Tarantini Stefano, Maier Andrea B., Csiszar Anna, Ungvari Zoltan
Dátum:	2025
ISSN:	2509-2715 2509-2723
Megjegyzések:	Abstract Aging remains the foremost risk factor for cardiovascular and cerebrovascular diseases, surpassing traditional factors in epidemiological signifcance. This review elucidates the cellular and molecular mechanisms underlying vascular aging, with an emphasis on sex diferences that infuence disease progression and clinical outcomes in older adults. We discuss the convergence of aging processes at the macro- and microvascular levels and their contributions to the pathogenesis of vascular diseases. Critical analysis of both preclinical and clinical studies reveals signifcant sex-specifc variations in these mechanisms, which could be pivotal in understanding the disparity in disease morbidity and mortality between sexes. The review highlights key molecular pathways, including oxidative stress, infammation, and autophagy, and their diferential roles in the vascular aging of males and females. We argue that recognizing these sex-specifc diferences is crucial for developing targeted therapeutic strategies aimed at preventing and managing age-related vascular pathologies. The implications for personalized medicine and potential areas for future research are also explored, emphasizing the need for a nuanced approach to the study and treatment of vascular aging.
Tárgyszavak:	Orvostudományok Elméleti orvostudományok idegen nyelvű folyóiratközlemény külföldi lapban folyóiratcikk Vascular aging Cellular senescence Menopause Endocrine Sex diferences Sexual dimorphism Atherosclerosis Vascular cognitive impairment Ischemic heart disease
Megjelenés:	GeroScience. - 47 : 1 (2025), p. 301-337. -
További szerzők:	Gulej, Rafal Patai Roland Papp Zoltán (1965-) (kardiológus, élettanász) Tóth Attila (1971-) (biológus) Szabó Attila Ádám (1996-) (orvos) Podesser, Bruno Karl Sótonyi Péter (1971-) (érsebész) (jr.) Benyó Zoltán Yabluchanskiy, Andriy Tarantini, Stefano Maier, Andrea B. Csiszár Anna Ungvári Zoltán
Pályázati támogatás:	EKÖP-2024-2 Egyéb EKÖP-2024-9 Egyéb National Institute on Aging (R01AG072295) Egyéb National Institute on Aging (R01AG055395) Egyéb National Institute on Aging (R01AG068295) Egyéb National Institute on Aging (R01AG070915) Egyéb National Institute of Neurological Disorders and Stroke (R01NS100782) Egyéb National Cancer Institute (R01CA255840) Egyéb TKP2021-NKTA-47 Egyéb National Cardiovascular Laboratory Program (RRF-2.3.1-21-2022-00003) Egyéb 101004093/ EUniWell/EAC-A02-2019 / EAC-A02-2019-1 Egyéb NKFIH Project no. 135784 Egyéb
Internet cím:	Szerző által megadott URL DOI Intézményi repozitóriumban (DEA) tárolt változat
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