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1.

001-es BibID:BIBFORM085461
035-os BibID:(WOS)000412737500001 (Scopus)85028747573
Első szerző:Csiszár Anna
Cím:Hypertension impairs neurovascular coupling and promotes microvascular injury : role in exacerbation of Alzheimer's disease / Csiszar Anna, Tarantini Stefano, Fülöp Gábor A., Kiss Tamas, Valcarcel-Ares M. Noa, Galvan Veronica, Ungvari Zoltan, Yabluchanskiy Andriy
Dátum:2017
ISSN:2509-2715 2509-2723
Megjegyzések:Hypertension in the elderly substantially increases both the risk of vascular cognitive impairment (VCI) and Alzheimer's disease (AD); however, the underlying mechanisms are not completely understood. This review discusses the effects of hypertension on structural and functional integrity of cerebral microcirculation, including hypertension-induced alterations in neurovascular coupling responses, cellular and molecular mechanisms involved in microvascular damage (capillary rarefaction, blood-brain barrier disruption), and the genesis of cerebral microhemorrhages and their potential role in exacerbation of cognitive decline associated with AD. Understanding and targeting the hypertension-induced cerebromicrovascular alterations that are involved in the onset and progression of AD and contribute to cognitive impairment are expected to have a major role in preserving brain health in high-risk older individuals.
Tárgyszavak:Orvostudományok Klinikai orvostudományok idegen nyelvű folyóiratközlemény külföldi lapban
folyóiratcikk
Functional hyperemia
Neurovascular coupling
Angiotensin II
High blood pressure
Hypertension
VCID
Endothelial dysfunction
Microcirculation
Alzheimer's disease
Megjelenés:GeroScience. - 39 : 4 (2017), p. 359-372. -
További szerzők:Tarantini, Stefano Fülöp Gábor Áron (1988-) (általános orvos) Kiss Tamás Valcarcel Ares, Marta Noa Galvan, Veronica Ungvári Zoltán Yabluchanskiy, Andriy
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2.

001-es BibID:BIBFORM076740
035-os BibID:(WoS)000462601700002 (Scopus)85062950434
Első szerző:Fülöp Gábor Áron (általános orvos)
Cím:IGF-1 Deficiency Promotes Pathological Remodeling of Cerebral Arteries : a Potential Mechanism Contributing to the Pathogenesis of Intracerebral Hemorrhages in Aging / Fulop Gabor A., Ramirez-Perez Francisco I., Kiss Tamas, Tarantini Stefano, Valcarcel Ares Marta Noa, Toth Peter, Yabluchanskiy Andriy, Conley Shannon M., Ballabh Praveen, Martinez-Lemus Luis A., Ungvari Zoltan, Csiszar Anna
Dátum:2019
ISSN:1079-5006
Tárgyszavak:Orvostudományok Klinikai orvostudományok idegen nyelvű folyóiratközlemény külföldi lapban
folyóiratcikk
Megjelenés:Journals Of Gerontology Series A-Biological Sciences And Medical Sciences. - 74 : 4 (2019), p. 446-454. -
További szerzők:Ramirez-Perez, Francisco I. Kiss Tamás Tarantini, Stefano Valcarcel Ares, Marta Noa Tóth Péter (sebész) Yabluchanskiy, Andriy Conley, Shannon M. Ballabh, Praveen Martinez-Lemus, Luis A. Ungvári Zoltán Csiszár Anna
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3.

001-es BibID:BIBFORM099949
035-os BibID:(WOS)000433040100011 (Scopus)85042217471
Első szerző:Tarantini, Stefano
Cím:Correction to : pharmacologically induced impairment of neurovascular coupling responses alters gait coordination in mice / Tarantini Stefano, Yabluchanskiy Andriy, Fülöp Gábor A., Hertelendy Peter, Noa Valcarcel-Ares M., Kiss Tamas, Bagwell Jonathan M., O'Connor Daniel, Farkas Eszter, Sorond Farzaneh, Csiszar Anna, Ungvari Zoltan
Dátum:2018
ISSN:2509-2715 2509-2723
Tárgyszavak:Orvostudományok Elméleti orvostudományok idegen nyelvű folyóiratközlemény külföldi lapban
folyóiratcikk
Megjelenés:GeroScience. - 40 : 2 (2018), p. 219-219. -
További szerzők:Yabluchanskiy, Andriy Fülöp Gábor Áron (1988-) (általános orvos) Hertelendy Péter Valcarcel Ares, Marta Noa Kiss Tamás (1950-) (vegyész) Bagwell, Jonathan M. O'Connor, Daniel Farkas Eszter Sorond, Farzaneh A. Csiszár Anna Ungvári Zoltán
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Intézményi repozitóriumban (DEA) tárolt változat
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4.

001-es BibID:BIBFORM085462
035-os BibID:(WOS)000418822500008 (Scopus)85038095208
Első szerző:Tarantini, Stefano
Cím:Pharmacologically induced impairment of neurovascular coupling responses alters gait coordination in mice / Tarantini Stefano, Yabluchanksiy Andriy, Fülöp Gábor A., Hertelendy Peter, Valcarcel-Ares M. Noa, Kiss Tamas, Bagwell Jonathan M., O'Connor Daniel. Farkas Eszter, Sorond Farzaneh, Csiszar Anna, Ungvari Zoltan
Dátum:2017
ISSN:2509-2715 2509-2723
Megjegyzések:There is correlative evidence that impaired cerebral blood flow (CBF) regulation, in addition to promoting cognitive impairment, is also associated with alterations in gait and development of falls in elderly people. CBF is adjusted to neuronal activity via neurovascular coupling (NVC) and this mechanism becomes progressively impaired with age. To establish a direct cause-andeffect relationship between impaired NVC and gait abnormalities, we induced neurovascular uncoupling pharmacologically in young C57BL/6 mice by inhibiting the synthesis of vasodilator mediators involved in NVC. Treatment of mice with the epoxygenase inhibitor MSPPOH, the NO synthase inhibitor L-NAME, and the COX inhibitor indomethacin significantly decreased NVC mimicking the aging phenotype. Pharmacologically induced neurovascular uncoupling significantly decreased the dynamic gait parameter duty cycle, altered footfall patterns, and significantly increased phase dispersion, indicating impaired interlimb coordination. Impaired NVC also tended to increase gait variability. Thus, selective experimental disruption of NVC causes subclinical gait abnormalities, supporting the importance of CBF in both cognitive function and gait regulation.
Tárgyszavak:Orvostudományok Klinikai orvostudományok idegen nyelvű folyóiratközlemény külföldi lapban
folyóiratcikk
Neurovascular coupling
Gait
Catwalk
Neurovascular uncoupling
Megjelenés:GeroScience. - 39 : 5-6 (2017), p. 601-614. -
További szerzők:Yabluchanskiy, Andriy Fülöp Gábor Áron (1988-) (általános orvos) Hertelendy Péter Valcarcel Ares, Marta Noa Kiss Tamás Bagwell, Jonathan M. O'Connor, Daniel Farkas Eszter Sorond, Farzaneh A. Csiszár Anna Ungvári Zoltán
Pályázati támogatás:EFOP-3.6.1-16-2016-00008
EFOP
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Intézményi repozitóriumban (DEA) tárolt változat
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5.

001-es BibID:BIBFORM085246
Első szerző:Tarantini, Stefano
Cím:Insulin-like growth factor 1 deficiency exacerbates hypertension-induced cerebral microhemorrhages in mice, mimicking the aging phenotype / Tarantini Stefano, Valcarcel-Ares Noa M., Yabluchanskiy Andriy, Springo Zsolt, Fulop Gabor A., Ashpole Nicole, Gautam Tripti, Giles Cory B., Wren Jonathan D., Sonntag William E., Csiszar Anna, Ungvari Zoltan
Dátum:2017
ISSN:1474-9718 1474-9726
Megjegyzések:Clinical and experimental studies show that aging exacerbates hypertension-induced cerebral microhemorrhages (CMHs), which progressively impair neuronal function. There is growing evidence that aging promotes insulin-like growth factor 1 (IGF-1) deficiency, which compromises multiple aspects of cerebromicrovascular and brain health. To determine the role of IGF-1 deficiency in the pathogenesis of CMHs, we induced hypertension in mice with liver-specific knockdown of IGF-1 (Igf1f/f + TBGCre-AAV8) and control mice by angiotensin II plus L-NAME treatment. In IGF-1-deficient mice, the same level of hypertension led to significantly earlier onset and increased incidence and neurological consequences of CMHs, as compared to control mice, as shown by neurological examination, gait analysis, and histological assessment of CMHs in serial brain sections. Previous studies showed that in aging, increased oxidative stressmediated matrix metalloprotease (MMP) activation importantly contributes to the pathogenesis of CMHs. Thus, it is significant that hypertension-induced cerebrovascular oxidative stress and MMP activation were increased in IGF-1-deficient mice. We found that IGF-1 deficiency impaired hypertension-induced adaptive media hypertrophy and extracellular matrix remodeling, which together with the increased MMP activation likely also contributes to increased fragility of intracerebral arterioles. Collectively, IGF-1 deficiency promotes the pathogenesis of CMHs, mimicking the aging phenotype, which likely contribute to its deleterious effect on cognitive function. Therapeutic strategies that upregulate IGF-1 signaling in the cerebral vessels and/or reduce microvascular oxidative stress, and MMP activation may be useful for the prevention of CMHs, protecting cognitive function in high-risk elderly patients.
Tárgyszavak:Orvostudományok Elméleti orvostudományok idegen nyelvű folyóiratközlemény külföldi lapban
folyóiratcikk
arteriole
dementia
gait dysfunction
microbleed
oxidative stress
Megjelenés:Aging Cell. - 16 : 3 (2017), p. 469-479. -
További szerzők:Valcarcel Ares, Marta Noa Yabluchanskiy, Andriy Springó Zsolt Fülöp Gábor Áron (1988-) (általános orvos) Ashpole, Nicole Gautam, Tripti Giles, Cory B. Wren, Jonathan D. Sonntag, William E. Csiszár Anna Ungvári Zoltán
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Intézményi repozitóriumban (DEA) tárolt változat
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6.

001-es BibID:BIBFORM076739
035-os BibID:(cikkazonosító)e12731 (WoS)000427234300020 (Scopus)85041585148
Első szerző:Tarantini, Stefano
Cím:Treatment with the mitochondrial-targeted antioxidant peptide SS-31 rescues neurovascular coupling responses and cerebrovascular endothelial function and improves cognition in aged mice / Stefano Tarantini, Noa M. Valcarcel-Ares, Andriy Yabluchanskiy, Gabor A. Fulop, Peter Hertelendy, Tripti Gautam, Eszter Farkas, Aleksandra Perz, Peter S. Rabinovitch, William E. Sonntag, Anna Csiszar, Zoltan Ungvari
Dátum:2018
ISSN:1474-9718
Megjegyzések:Moment-to-moment adjustment of cerebral blood flow (CBF) via neurovascular coupling has an essential role in maintenance of healthy cognitive function. In advanced age, increased oxidative stress and cerebromicrovascular endothelial dysfunction impair neurovascular coupling, likely contributing to age-related decline of higher cortical functions. There is increasing evidence showing that mitochondrial oxidative stress plays a critical role in a range of age-related cellular impairments, but its role in neurovascular uncoupling remains unexplored. This study was designed to test the hypothesis that attenuation of mitochondrial oxidative stress may exert beneficial effects on neurovascular coupling responses in aging. To test this hypothesis, 24-month-old C57BL/6 mice were treated with a cell-permeable, mitochondria-targeted antioxidant peptide (SS-31; 10 mg kg-1 day-1 , i.p.) or vehicle for 2 weeks. Neurovascular coupling was assessed by measuring CBF responses (laser speckle contrast imaging) evoked by contralateral whisker stimulation. We found that neurovascular coupling responses were significantly impaired in aged mice. Treatment with SS-31 significantly improved neurovascular coupling responses by increasing NO-mediated cerebromicrovascular dilation, which was associated with significantly improved spatial working memory, motor skill learning, and gait coordination. These findings are paralleled by the protective effects of SS-31 on mitochondrial production of reactive oxygen species and mitochondrial respiration in cultured cerebromicrovascular endothelial cells derived from aged animals. Thus, mitochondrial oxidative stress contributes to age-related cerebromicrovascular dysfunction, exacerbating cognitive decline. We propose that mitochondria-targeted antioxidants may be considered for pharmacological microvascular protection for the prevention/treatment of age-related vascular cognitive impairment (VCI).
Tárgyszavak:Orvostudományok Klinikai orvostudományok idegen nyelvű folyóiratközlemény külföldi lapban
folyóiratcikk
aging
cerebral circulation
endothelial dysfunction
oxidative stress
vascular cognitive impairment
Megjelenés:Aging Cell. - 17 : 2 (2018), p. 1-12. -
További szerzők:Valcarcel Ares, Marta Noa Yabluchanskiy, Andriy Fülöp Gábor Áron (1988-) (általános orvos) Hertelendy Péter Gautam, Tripti Farkas Eszter Perz, Aleksandra Rabinovitch, Peter S. Sonntag, William E. Csiszár Anna Ungvári Zoltán
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Intézményi repozitóriumban (DEA) tárolt változat
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7.

001-es BibID:BIBFORM085446
035-os BibID:(WOS)000401331200004 (Scopus)85017238534
Első szerző:Ungvári Zoltán
Cím:Cerebromicrovascular dysfunction predicts cognitive decline and gait abnormalities in a mouse model of whole brain irradiation-induced accelerated brain senescence / Ungvari Zoltan, Tarantini Stefano, Hertelendy Peter, Valcarcel-Ares M. Noa, Fülöp Gabor A., Logan Sreemathi, Kiss Tamas, Farkas Eszter, Csiszar Anna, Yabluchanskiy Andriy
Dátum:2017
ISSN:2509-2715 2509-2723
Megjegyzések:Whole brain irradiation (WBI) is a mainstream therapy for patients with both identifiable brain metastases and prophylaxis for microscopic malignancies. However, it also promotes accelerated senescence in healthy tissues and leads to progressive cognitive dysfunction in up to 50% of tumor patients surviving long term after treatment, due to ?-irradiation-induced cerebromicrovascular injury. Moment-to-moment adjustment of cerebral blood flow (CBF) via neuronal activity-dependent cerebromicrovascular dilation (functional hyperemia) has a critical role in maintenance of healthy cognitive function. To determine whether cognitive decline induced by WBI associates with impaired cerebromicrovascular function, C56BL/6 mice (3 months) subjected to a clinically relevant protocol of fractionated WBI (5 Gy twice weekly for 4 weeks) and control mice were compared. Mice were tested for spatial memory performance (radial arm water maze), sensorimotor coordination (computerized gait analysis, CatWalk), and cerebromicrovascular function (whisker-stimulation-induced increases in CBF, measured by laser Doppler flowmetry) at 3 to 6 months post-irradiation. We found that mice with WBI exhibited impaired cerebromicrovascular function at 3 months post-irradiation, which was associated with impaired performance in the radial arm water maze. At 6 months, post-irradiation progressive impairment in gait coordination (including changes in the regularity index and phase dispersion) was also evident. Collectively, our findings provide evidence for early and persisting neurovascular impairment after a clinically relevant protocol of fractionated WBI, which predict early manifestations of cognitive impairment.
Tárgyszavak:Orvostudományok Klinikai orvostudományok idegen nyelvű folyóiratközlemény külföldi lapban
folyóiratcikk
Whole brain irradiation
Neurovascular coupling
Functional hyperemia
Dementia
Gait dysfunction
Neurovascular unit
Cellular senescence
DNA damage
Megjelenés:GeroScience. - 39 : 1 (2017), p. 33-42. -
További szerzők:Tarantini, Stefano Hertelendy Péter Valcarcel Ares, Marta Noa Fülöp Gábor Áron (1988-) (általános orvos) Logan, Sreemathi Kiss Tamás Farkas Eszter Csiszár Anna Yabluchanskiy, Andriy
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Intézményi repozitóriumban (DEA) tárolt változat
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8.

001-es BibID:BIBFORM085464
035-os BibID:(WOS)000418822500002 (Scopus)85028959893
Első szerző:Ungvári Zoltán
Cím:Connective tissue growth factor (CTGF) in age-related vascular pathologies / Ungvari Zoltan, Valcarcel-Ares Marta Noa, Tarantini Stefano, Yabluchanskiy Andriy, Fülöp Gábor A., Kiss Tamas, Csiszar Anna
Dátum:2017
ISSN:2509-2715 2509-2723
Megjegyzések:Connective tissue growth factor (CTGF, also known as CCN2) is a matricellular protein expressed in the vascular wall, which regulates diverse cellular functions including cell adhesion, matrix production, structural remodeling, angiogenesis, and cell proliferation and differentiation. CTGF is principally regulated at the level of transcription and is induced by mechanical stresses and a number of cytokines and growth factors, including TGF?. In this mini-review, the role of age-related dysregulation of CTGF signaling and its role in a range of macro- and microvascular pathologies, including pathogenesis of aorta aneurysms, atherogenesis, and diabetic retinopathy, are discussed. A potential role of CTGF and TGF? in regulation and non-cell autonomous propagation of cellular senescence is also discussed.
Tárgyszavak:Orvostudományok Klinikai orvostudományok idegen nyelvű folyóiratközlemény külföldi lapban
folyóiratcikk
CTGF
Extracellular matrix
Cerebromicrovascular
Vascular aging
Megjelenés:GeroScience. - 39 : 5-6 (2017), p. 491-498. -
További szerzők:Valcarcel Ares, Marta Noa Tarantini, Stefano Yabluchanskiy, Andriy Fülöp Gábor Áron (1988-) (általános orvos) Kiss Tamás Csiszár Anna
Pályázati támogatás:EFOP-3.6.1-16-2016-00008
EFOP
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Intézményi repozitóriumban (DEA) tárolt változat
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