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1.

001-es BibID:BIBFORM108755
035-os BibID:(scopus)85146738441 (WOS)000922305000002
Első szerző:Berkowicz, Piotr
Cím:Accelerated ageing and coronary microvascular dysfunction in chronic heart failure in Tgαq*44 mice / Berkowicz Piotr, Totoń-Żurańska Justyna, Kwiatkowski Grzegorz, Jasztal Agnieszka, Csípő Tamás, Kus Kamil, Tyrankiewicz Urszula, Orzyłowska Anna, Wołkow Paweł, Tóth Attila, Chlopicki Stefan
Dátum:2023
ISSN:2509-2715 2509-2723
Tárgyszavak:Orvostudományok Klinikai orvostudományok idegen nyelvű folyóiratközlemény külföldi lapban
folyóiratcikk
Megjelenés:GeroScience. - 45 : 3 (2023), p. 1619-1648. -
További szerzők:Totoń-Żurańska, Justyna Kwiatkowski, Grzegorz Jasztal, Agnieszka Csípő Tamás (1990-) Kus, Kamil Tyrankiewicz, Urszula Orzyłowska, Anna Wołkow, Paweł Tóth Attila (1971-) (biológus) Chlopicki, Stefan
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Intézményi repozitóriumban (DEA) tárolt változat
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2.

001-es BibID:BIBFORM099947
035-os BibID:(WOS)000493706100001 (Scopus)85074834329
Első szerző:Csípő Tamás
Cím:Assessment of age-related decline of neurovascular coupling responses by functional near-infrared spectroscopy (fNIRS) in humans / Csipo Tamas, Mukli Peter, Lipecz Agnes, Tarantini Stefano, Bahadli Dhay, Abdulhussein Osamah, Owens Cameron, Kiss Tamas, Balasubramanian Priya, Nyúl-Tóth Ádám, Hand Rachel A., Yabluchanska Valeriya, Sorond Farzaneh A., Csiszar Anna, Ungvari Zoltan, Yabluchanskiy Andriy
Dátum:2019
ISSN:2509-2715 2509-2723
Megjegyzések:Preclinical studies provide strong evidence that age-related impairment of neurovascular coupling (NVC) plays a causal role in the pathogenesis of vascular cognitive impairment (VCI). NVC is a critical homeostatic mechanism in the brain, responsible for adjustment of local cerebral blood flow to the energetic needs of the active neuronal tissue. Recent progress in geroscience has led to the identification of critical cellular and molecular mechanisms involved in neurovascular aging, identifying these pathways as targets for intervention. In order to translate the preclinical findings to humans, there is a need to assess NVC in geriatric patients as an endpoint in clinical studies. Functional near-infrared spectroscopy (fNIRS) is a non-invasive neuroimaging technique that enables the investigation of local changes in cerebral blood flow, quantifying task-related changes in oxygenated and deoxygenated hemoglobin concentrations. In the present overview, the basic principles of fNIRS are introduced and the application of this technique to assess NVC in older adults with implications for the design of studies on the mechanistic underpinnings of VCI is discussed.
Tárgyszavak:Orvostudományok Elméleti orvostudományok idegen nyelvű folyóiratközlemény külföldi lapban
folyóiratcikk
Aging
Cognitive aging
Functional near-infrared spectroscopy
Neurovascular coupling
VCI
VCID
Vascular cognitive impairment and dementia
fNIRS
Megjelenés:GeroScience. - 41 : 5 (2019), p. 495-509. -
További szerzők:Mukli Péter Lipécz Ágnes Tarantini, Stefano Bahadli, Dhay Abdulhussein, Osamah Owens, Cameron D. Kiss Tamás (1950-) (vegyész) Balasubramanian, Priya Nyúl-Tóth Ádám Hand, Rachel A. Yabluchanska, Valeriya Sorond, Farzaneh A. Csiszár Anna Ungvári Zoltán Yabluchanskiy, Andriy
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Intézményi repozitóriumban (DEA) tárolt változat
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3.

001-es BibID:BIBFORM099943
035-os BibID:(WOS)000469877700003 (Scopus)85066471327
Első szerző:Csípő Tamás
Cím:Age-related decline in peripheral vascular health predicts cognitive impairment / Csipo Tamas, Lipecz Agnes, Fulop Gabor A., Hand Rachel A., Ngo Bich-Thy N., Dzialendzik Mikita, Tarantini Stefano, Balasubramanian Priya, Kiss Tamas, Yabluchanska Valeriya, Silva-Palacios Federico, Courtney Donald L., Dasari Tarun W., Sorond Farzaneh, Sonntag William E., Csiszar Anna, Ungvari Zoltan, Yabluchanskiy Andriy
Dátum:2019
ISSN:2509-2715 2509-2723
Megjegyzések:Preclinical studies demonstrate that generalized endothelial cell dysfunction and microvascular impairment are potentially reversible causes of age-related vascular cognitive impairment and dementia (VCID). The present study was designed to test the hypothesis that severity of age-related macro- and microvascular dysfunction measured in the peripheral circulation is an independent predictor of cognitive performance in older adults. In this study, we enrolled 63 healthy individuals into young (< 45 years old) and aged (> 65 years old) groups. We used principal component analysis (PCA) to construct a comprehensive peripheral vascular health index (VHI) encompassing peripheral microvascular reactivity, arterial endothelial function, and vascular stiffness, as a marker of aging-induced generalized vascular dysfunction. Peripheral macrovascular and microvascular endothelial function were assessed using flow-mediated dilation (FMD) and laser speckle contrast imaging tests. Pulse waveform analysis was used to evaluate the augmentation index (AIx), a measure of arterial stiffness. Cognitive function was measured using a panel of CANTAB cognitive tests, and PCA was then applied to generate a cognitive impairment index (CII) for each participant. Aged subjects exhibited significantly impaired macrovascular endothelial function (FMD, 5.6 ? 0.7% vs. 8.3 ? 0.6% in young, p = 0.0061), increased arterial stiffness (AIx 29.3 ? 1.8% vs 4.5 ? 2.6% in young, p < 0.0001), and microvascular dysfunction (2.8 ? 0.2 vs 3.4 ? 0.1-fold change of perfusion in young, p = 0.032). VHI showed a significant negative correlation with age (r = - 0.54, p < 0.0001) and CII significantly correlated with age (r = 0.79, p < 0.0001). VHI significantly correlated with the CII (r = - 0.46, p = 0.0003). A decline in peripheral vascular health may reflect generalized vascular dysfunction and predict cognitive impairment in older adults.
Tárgyszavak:Orvostudományok Elméleti orvostudományok idegen nyelvű folyóiratközlemény külföldi lapban
folyóiratcikk
Aging
Endothelial function
Cognitive impairment
Microvascular dysfunction
VCID
Megjelenés:GeroScience. - 41 : 2 (2019), p. 125-136. -
További szerzők:Lipécz Ágnes Fülöp Gábor Áron (1988-) (általános orvos) Hand, Rachel A. Ngo, Bich-Thy N. Dzialendzik, Mikita Tarantini, Stefano Balasubramanian, Priya Kiss Tamás (1950-) (vegyész) Yabluchanska, Valeriya Silva-Palacios, Federico Courtney, Donald L. Dasari, Tarun W. Sorond, Farzaneh A. Sonntag, William E. Csiszár Anna Ungvári Zoltán Yabluchanskiy, Andriy
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Intézményi repozitóriumban (DEA) tárolt változat
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4.

001-es BibID:BIBFORM076737
035-os BibID:(WOS)000440106900010 (Scopus)85048661448
Első szerző:Csípő Tamás
Cím:Short-term weight loss reverses obesity-induced microvascular endothelial dysfunction / Tamas Csipo, Gabor A. Fulop, Agnes Lipecz, Stefano Tarantini, Tamas Kiss, Priya Balasubramanian, Anna Csiszar, Zoltan Ungvari, Andriy Yabluchanskiy
Dátum:2018
ISSN:2509-2715 2509-2723
Megjegyzések:Obesity is one of the major risk factors for cardiovascular diseases and its prevalence is increasing in all age groups, with the biggest impact observed in middle-aged and older adults. A critical mechanism by which obesity promotes vascular pathologies in these patients involves impairment of endothelial function. While endothelial dysfunction in large vessels promotes atherogenesis, obesity-induced microvascular endothelial dysfunction impairs organ perfusion and thereby is causally related to the pathogenesis of ischemic heart disease, chronic kidney disease, intermittent claudication, exercise intolerance, and exacerbates cognitive decline in aging. Reduction of weight via calorie-based diet and exercise in animal models of obesity results in significant improvement of endothelial function both in large vessels and in the microcirculation, primarily due to attenuation of oxidative stress and inflammation. Clinical data on the protective effects of weight loss on endothelial function is limited to studies of flow-mediated dilation assessed in brachial arteries. Currently, there is no guideline on testing the effects of different weight management strategies on microvascular endothelial function in obese patients. Here, we provide proof-of-concept that weight loss-induced improvement of microvascular endothelial function can be reliably assessed in the setting of a geriatric outpatient clinic using a fast, reproducible, non-invasive method: laser speckle contrast imaging-based measurement of endothelium-dependent microvascular responses during post-occlusive reactive hyperemia tests. Our study also provides initial evidence that short-term weight loss induced by consumption of a low-carbohydrate low-calorie diet can reverse microvascular endothelial dysfunction associated with obesity.
Tárgyszavak:Orvostudományok Klinikai orvostudományok idegen nyelvű folyóiratközlemény külföldi lapban
folyóiratcikk
Weight loss
Obesity
Endothelial function
Aging
Megjelenés:GeroScience. - 40 : 3 (2018), p. 337-346. -
További szerzők:Fülöp Gábor Áron (1988-) (általános orvos) Lipécz Ágnes Tarantini, Stefano Kiss Tamás Balasubramanian, Priya Csiszár Anna Ungvári Zoltán Yabluchanskiy, Andriy
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Intézményi repozitóriumban (DEA) tárolt változat
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5.

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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Intézményi repozitóriumban (DEA) tárolt változat
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6.

001-es BibID:BIBFORM103836
035-os BibID:(wos)000854410800001 (Scopus)85138156081
Első szerző:Fagyas Miklós (orvos)
Cím:The majority of severe COVID-19 patients develop anti-cardiac autoantibodies / Fagyas Miklós, Nagy Béla, Ráduly Arnold Péter, Mányiné Siket Ivetta, Mártha Lilla, Erdősi Gábor, Sipka Sándor, Enyedi Enikő, Szabó Attila Ádám, Pólik Zsófia, Kappelmayer János, Papp Zoltán, Borbély Attila, Szabó Tamás, Balla József, Balla György, Bai Péter, Bácsi Attila, Tóth Attila
Dátum:2022
ISSN:2509-2715 2509-2723
Megjegyzések:Severe cases of COVID-19 are characterized by an inflammatory burst, which is accompanied by multiorgan failure. The elderly population has higher risk for severe or fatal outcome for COVID-19. Inflammatory mediators facilitate the immune system to combat viral infection by producing antibodies against viral antigens. Several studies reported that the pro-inflammatory state and tissue damage in COVID-19 also promotes autoimmunity by autoantibody generation. We hypothesized that a subset of these autoantibodies targets cardiac antigens. Here we aimed to detect anti-cardiac autoantibodies in severe COVID-19 patients during hospitalization. For this purpose, 104 COVID-19 patients were recruited, while 40 heart failure patients with dilated cardiomyopathy and 20 patients with severe aortic stenosis served as controls. Patients were tested for anti-cardiac autoantibodies, using human heart homogenate as a bait. Follow-up samples were available in 29 COVID-19 patients. Anti-cardiac autoantibodies were detected in 68% (71 out of 104) of severe COVID-19 patients. Overall, 39% of COVID-19 patients had anti-cardiac IgG autoantibodies, while 51% had anti-cardiac autoantibodies of IgM isotype. Both IgG and IgM anti-cardiac autoantibodies were observed in 22% of cases, and multiple cardiac antigens were targeted in 38% of COVID-19 patients. These anti-cardiac autoantibodies targeted a diverse set of myocardial proteins, without apparent selectivity. As controls, heart failure patients (with dilated cardiomyopathy) had similar occurrence of IgG (45%, p = 0.57) autoantibodies, while significantly lower occurrence of IgM autoantibodies (30%, p = 0.03). Patients with advanced aortic stenosis had significantly lower number of both IgG (11%, p = 0.03) and IgM (10%, p < 0.01) type anti-cardiac autoantibodies than that in COVID-19 patients. Furthermore, we detected changes in the anti-cardiac autoantibody profile in 7 COVID-19 patients during hospital treatment. Surprisingly, the presence of these anti-cardiac autoantibodies did not affect the clinical outcome and the prevalence of the autoantibodies did not differ between the elderly (over 65 years) and the patients younger than 65 years of age. Our results demonstrate that the majority of hospitalized COVID-19 patients produce novel anti-cardiac IgM autoantibodies. COVID-19 also reactivates resident IgG autoantibodies. These autoantibodies may promote autoimmune reactions, which can complicate post-COVID recuperation, contributing to post-acute sequelae of COVID-19 (long COVID).
Tárgyszavak:Orvostudományok Elméleti orvostudományok idegen nyelvű folyóiratközlemény külföldi lapban
folyóiratcikk
COVID-19
Anti-cardiac autoantibodies
SARS-CoV-2
Megjelenés:GeroScience. - 44 (2022), p. 2347-2360. -
További szerzők:Nagy Béla Jr. (1980-) (labordiagnosztikai szakorvos) Ráduly Arnold Péter (1993-) Mányiné Siket Ivetta (1962-) (laborasszisztens) Mártha Lilla Erdősi Gábor Sipka Sándor ifj. (1980-) (orvos) Enyedi Enikő Edit (1995-) (orvosi laboratóriumi analitikus) Szabó Attila Ádám (1996-) (orvos) Pólik Zsófia Kappelmayer János (1960-) (laboratóriumi szakorvos) Papp Zoltán (1965-) (kardiológus, élettanász) Borbély Attila (1978-) (kardiológus) Szabó Tamás (1968-) (gyermekgyógyász) Balla József (1959-) (belgyógyász, nephrológus) Balla György (1953-) (csecsemő és gyermekgyógyász, neonatológus) Bai Péter (1976-) (biokémikus) Bácsi Attila (1967-) (immunológus) Tóth Attila (1971-) (biológus)
Pályázati támogatás:GINOP-2.3.2-15-2016-00050
GINOP
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Intézményi repozitóriumban (DEA) tárolt változat
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7.

001-es BibID:BIBFORM096668
035-os BibID:(WOS)000709656800002 (Scopus)85116969228
Első szerző:Fagyas Miklós (orvos)
Cím:Changes in the SARS-CoV-2 cellular receptor ACE2 levels in cardiovascular patients : a potential biomarker for the stratification of COVID-19 patients / Miklós Fagyas, Viktor Bánhegyi, Katalin Úri, Attila Enyedi, Erzsébet Lizanecz, Ivetta Mányiné Siket, Lilla Mártha, Gábor Áron Fülöp, Tamás Radovits, Miklós Pólos, Béla Merkely, Árpád Kovács, Zoltán Szilvássy, Zoltán Ungvári, István Édes, Zoltán Csanádi, Judit Boczán, István Takács, Gábor Szabó, József Balla, György Balla, Petar Seferovic, Zoltán Papp, Attila Tóth
Dátum:2021
ISSN:2509-2715 2509-2723
Tárgyszavak:Orvostudományok Elméleti orvostudományok idegen nyelvű folyóiratközlemény külföldi lapban
folyóiratcikk
SARS-CoV-2
ACE2
COVID-19
biomarker
cardiovascular
Megjelenés:GeroScience. - 43 : 5 (2021), p. 2289-2304. -
További szerzők:Bánhegyi Viktor (1991-) (kardiológus) Úri Katalin Enyedi Attila (1975-) (sebész) Lizanecz Erzsébet (1978-) (orvos) Mányiné Siket Ivetta (1962-) (laborasszisztens) Mártha Lilla Fülöp Gábor Áron (1988-) (általános orvos) Radovits Tamás Pólos Miklós Merkely Béla (1965-) (orvos) Kovács Árpád (1986-) (kardiológus) Szilvássy Zoltán (1957-) (belgyógyász, farmakológus, klinikai farmakológus) Ungvári Zoltán Édes István (1952-) (kardiológus) Csanádi Zoltán (1960-) (kardiológus) Boczán Judit (1972-) (neurológus) Takács István (1963-) (sebész) Szabó Gábor Balla József (1959-) (belgyógyász, nephrológus) Balla György (1953-) (csecsemő és gyermekgyógyász, neonatológus) Seferović, Petar M. Papp Zoltán (1965-) (kardiológus, élettanász) Tóth Attila (1971-) (biológus)
Pályázati támogatás:GINOP-2.3.2-15-2016-00043
GINOP
GINOP-2.3.2-15-2016-00050
EFOP-3.6.2-16-2017-00006
EFOP
NKFIH - K134939
Egyéb
NKFIH - FK128809
Egyéb
NKFIH - K116940
Egyéb
NKFIH - K132623
Egyéb
NVKP_16-1-2016-0017
Egyéb
2020-4.1.1.-TKP2020
Egyéb
TKP2020-NKA-04
Egyéb
Internet cím:Intézményi repozitóriumban (DEA) tárolt változat
DOI
Borító:

8.

001-es BibID:BIBFORM090205
035-os BibID:(WOS)000608951800001 (Scopus)85099552143
Első szerző:Fagyas Miklós (orvos)
Cím:Level of the SARS-CoV-2 receptor ACE2 activity is highly elevated in old-aged patients with aortic stenosis : implications for ACE2 as a biomarker for the severity of COVID-19 / Fagyas Miklós, Kertész Attila, Mányiné Siket Ivetta, Bánhegyi Viktor, Kracskó Bertalan, Szegedi Andrea, Szokol Miklós, Vajda Gusztáv, Rácz Ildikó, Gulyás Hajnalka, Szkibák Noémi, Rácz Vivien, Csanádi Zoltán, Papp Zoltán, Tóth Attila, Sipka Sándor
Dátum:2021
ISSN:2509-2715 2509-2723
Megjegyzések:Coronavirus disease 2019 (COVID-19) has a high mortality in elderly patients with preexisting cardiovascular diseases. The cellular receptor of severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2) is the angiotensin converting enzyme 2 (ACE2), thereby implicating a link between cardiovascular diseases and SARS-CoV-2 susceptibility. Aortic stenosis (AS) represents a chronic inflammatory state with severe cardiovascular complications in the elderly, a prime condition for COVID-19 mortality. The circulating ACE2 levels were measured in 111 patients with severe AS and compared to patients with hypertension and healthy individuals. About 4-times higher circulating ACE2 activity was found in patients with severe AS than in hypertensives or healthy individuals (88.3?61.6., n=111, 20.6?13.4, n=540 and 16.1?7.4 mU/L, n=46, respectively). Patients with severe AS were older than patients with hypertension (80?6 years vs. 60?15 years, P<0.05). Serum ACE2 activity correlated negatively with the left ventricular ejection fraction, aortic root area, TAPSE and positively with the right ventricular systolic pressure, cardiac diameters in patients with AS. In contrast, circulating ACE2 activity was independent of the blood pressure, peak flow velocity at the aortic root, kidney function (GFR) and inflammatory state (CRP). We found no effect of RAAS inhibitory drugs on the serum ACE2 activity in this group of patients. Our results illustrate circulating ACE2 as a potential interface between chronic inflammation, cardiovascular disease and COVID-19 susceptibility. Elderly patients with AS have markedly elevated ACE2 levels together with altered left and right ventricular functions, which may pose higher risks during COVID-19. Our clinical data do not support a role for RAAS inhibitors in regulating circulating ACE2 levels.
taa, km
Tárgyszavak:Orvostudományok Elméleti orvostudományok idegen nyelvű folyóiratközlemény külföldi lapban
folyóiratcikk
ACE2
TAVI
COVID-19
aortic stenosis
age
Megjelenés:GeroScience. - 43 : 1 (2021), p. 19-29. -
További szerzők:Kertész Attila Béla (1973-) (kardiológus) Mányiné Siket Ivetta (1962-) (laborasszisztens) Bánhegyi Viktor (1991-) (kardiológus) Kracskó Bertalan (1986-) (orvos) Szegedi Andrea (kardiológus) Szokol Miklós (1971-) (kardiológus) Vajda Gusztáv (1956-) (kardiológus) Rácz Ildikó (1973-) (kardiológus) Gulyás Hajnalka Szkibák Noémi Rácz Vivien Csanádi Zoltán (1960-) (kardiológus) Papp Zoltán (1965-) (kardiológus, élettanász) Tóth Attila (1971-) (biológus) Sipka Sándor ifj. (1980-) (orvos)
Pályázati támogatás:GINOP-2.3.2-15-2016-00043
GINOP
EFOP-3.6.2-16-2017-00006
EFOP
GINOP-2.3.2-15-2016-00050
GINOP
OTKA-116940
OTKA
NKFIH-K132623
Egyéb
NKFIH-FK128809
Egyéb
ED_18-1-2019-0028
Egyéb
Internet cím:DOI
Intézményi repozitóriumban (DEA) tárolt változat
Borító:

9.

001-es BibID:BIBFORM082128
035-os BibID:(WOS)000494370900001 (Scopus)85074926339
Első szerző:Fülöp Gábor Áron (általános orvos)
Cím:Cerebral venous congestion promotes blood-brain barrier disruption and neuroinflammation, impairing cognitive function in mice / Gabor A. Fulop, Chetan Ahire, Tamas Csipo, Stefano Tarantini, Tamas Kiss, Priya Balasubramanian, Andriy Yabluchanskiy, Eszter Farkas, Attila Toth, Ádám Nyúl-Tóth, Peter Toth, Anna Csiszar, Zoltan Ungvari
Dátum:2019
ISSN:2509-2715 2509-2723
Tárgyszavak:Orvostudományok Klinikai orvostudományok idegen nyelvű folyóiratközlemény külföldi lapban
folyóiratcikk
Megjelenés:GeroScience. - 41 : 5 (2019), p. 575-589. -
További szerzők:Ahire, Chetan Csípő Tamás (1990-) Tarantini, Stefano Kiss Tamás Balasubramanian, Priya Yabluchanskiy, Andriy Farkas Eszter Tóth Attila (1971-) (biológus) Nyúl-Tóth Ádám Tóth Péter Csiszár Anna Ungvári Zoltán
Pályázati támogatás:EFOP-3.6.1-16-2016-00008, 20765-3/2018/FEKUTSTRAT
EFOP
EFOP-3.6.2.-16-2017-00008
EFOP
GINOP-2.3.2-15-2016-00048
GINOP
GINOP-2.3.3-15-2016-00032
GINOP
NKFI-FK123798
NKFIH
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DOI
Intézményi repozitóriumban (DEA) tárolt változat
Borító:

10.

001-es BibID:BIBFORM076738
035-os BibID:(WOS)000453351000007 (Scopus)85057166811
Első szerző:Fülöp Gábor Áron (általános orvos)
Cím:Nrf2 deficiency in aged mice exacerbates cellular senescence promoting cerebrovascular inflammation / Gabor A. Fulop, Tamas Kiss, Stefano Tarantini, Priya Balasubramanian, Andriy Yabluchanskiy, Eszter Farkas, Ferenc Bari, Zoltan Ungvari, Anna Csiszar
Dátum:2018
ISSN:2509-2715 2509-2723
Megjegyzések:Aging-induced pro-inflammatory phenotypic alterations of the cerebral vasculature critically contribute to the pathogenesis of vascular cognitive impairment. Cellular senescence is a fundamental aging process that promotes inflammation; however, its role in cerebrovascular aging remains unexplored. The present study was undertaken to test the hypothesis that advanced aging promotes cellular senescence in the cerebral vasculature. We found that in cerebral arteries of 24-month-old mice, expression of molecular markers of senescence (p16INK4a, p21) is upregulated as compared to that in young controls. Induction of senescence programs in cerebral arteries is associated by an upregulation of a wide range of inflammatory cytokines and chemokines, which are known to contribute to the senescence-associated secretory phenotype (SASP) in vascular cells. Age-related cerebrovascular senescence and inflammation are associated with neuroinflammation, as shown by the molecular footprint of microglia activation in the hippocampus. Genetic depletion of the pro-survival/anti-aging transcriptional regulator Nrf2 exacerbated age-related induction of senescence markers and inflammatory SASP factors and resulted in a heightened inflammatory status of the hippocampus. In conclusion, our studies provide evidence that aging and Nrf2 dysfunction promote cellular senescence in cerebral vessels, which may potentially cause or exacerbate age-related pathology.
Tárgyszavak:Orvostudományok Klinikai orvostudományok idegen nyelvű folyóiratközlemény külföldi lapban
folyóiratcikk
Endothelial dysfunction
Senescence
VCID
Vascular aging
Vascular cognitive impairment
Megjelenés:GeroScience. - 40 : 5-6 (2018), p. 513-521. -
További szerzők:Kiss Tamás Tarantini, Stefano Balasubramanian, Priya Yabluchanskiy, Andriy Farkas Eszter Bari Ferenc Ungvári Zoltán Csiszár Anna
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DOI
Intézményi repozitóriumban (DEA) tárolt változat
Borító:

11.

001-es BibID:BIBFORM099929
035-os BibID:(WOS)000531041500024 (Scopus)85082710654
Első szerző:Kiss Tamás (vegyész)
Cím:Circulating anti-geronic factors from heterochonic parabionts promote vascular rejuvenation in aged mice : transcriptional footprint of mitochondrial protection, attenuation of oxidative stress, and rescue of endothelial function by young blood / Kiss Tamas, Tarantini Stefano, Csipo Tamas, Balasubramanian Priya, Nyúl-Tóth Ádám, Yabluchanskiy Andriy, Wren Jonathan D., Garman Lori, Huffman Derek M., Csiszar Anna, Ungvari Zoltan
Dátum:2020
ISSN:2509-2715 2509-2723
Megjegyzések:Aging-induced functional and phenotypic alterations of the vasculature (e.g., endothelial dysfunction, oxidative stress) have a central role in morbidity and mortality of older adults. It has become apparent in recent years that cell autonomous mechanisms alone are inadequate to explain all aspects of vascular aging. The present study was designed to test the hypothesis that age-related changes in circulating anti-geronic factors contribute to the regulation of vascular aging processes in a non-cell autonomous manner. To test this hypothesis, through heterochronic parabiosis we determined the extent, if any, to which endothelial function, vascular production of ROS, and shifts in the vascular transcriptome (RNA-seq) are modulated by the systemic environment. We found that in aortas isolated from isochronic parabiont aged (20-month-old) C57BL/6 mice [A-(A); parabiosis for 8 weeks] acetylcholine-induced endothelium-dependent relaxation was impaired and ROS production (dihydroethidium fluorescence) was increased as compared with those in aortas from young isochronic parabiont (6-month-old) mice [Y-(Y)]. The presence of young blood derived from young parabionts significantly improved endothelium-dependent vasorelaxation and attenuated ROS production in vessels of heterochronic parabiont aged [A-(Y)] mice. In aortas derived from heterochronic parabiont young [Y-(A)] mice, acetylcholine-induced relaxation and ROS production were comparable with those in aortas derived from Y-(Y) mice. Using RNA-seq we assessed transcriptomic changes in the aortic arch associated with aging and heterochronic parabiosis. We identified 347 differentially expressed genes in A-(A) animals compared with Y-(Y) controls. We have identified 212 discordant genes, whose expression levels differed in the aged phenotype, but have shifted back toward the young phenotype by the presence of young blood in aged A-(Y) animals. Pathway analysis shows that vascular protective effects mediated by young blood-regulated genes include mitochondrial rejuvenation. In conclusion, a relatively short-term exposure to young blood can rescue vascular aging phenotypes, including attenuation of oxidative stress, mitochondrial rejuvenation, and improved endothelial function. Our findings provide additional evidence supporting the significant plasticity of vascular aging and evidence for the existence of anti-geronic factors capable of exerting rejuvenating effects on the aging vasculature.
Tárgyszavak:Orvostudományok Elméleti orvostudományok idegen nyelvű folyóiratközlemény külföldi lapban
folyóiratcikk
Megjelenés:GeroScience. - 42 : 2 (2020), p. 727-748. -
További szerzők:Tarantini, Stefano Csípő Tamás (1990-) Balasubramanian, Priya Nyúl-Tóth Ádám Yabluchanskiy, Andriy Wren, Jonathan D. Garman, Lori Huffman, Derek M. Csiszár Anna Ungvári Zoltán
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DOI
Intézményi repozitóriumban (DEA) tárolt változat
Borító:

12.

001-es BibID:BIBFORM099926
035-os BibID:(WOS)000522703800001 (Scopus)85083217977
Első szerző:Kiss Tamás (vegyész)
Cím:Single-cell RNA sequencing identifies senescent cerebromicrovascular endothelial cells in the aged mouse brain / Kiss Tamas, Nyúl-Tóth Ádám, Balasubramanian Priya, Tarantini Stefano, Ahire Chetan, DelFavero Jordan, Yabluchanskiy Andriy, Csipo Tamas, Farkas Eszter, Wiley Graham, Garman Lori, Csiszar Anna, Ungvari Zoltan
Dátum:2020
ISSN:2509-2715 2509-2723
Megjegyzések:Age-related phenotypic changes of cerebromicrovascular endothelial cells lead to dysregulation of cerebral blood flow and blood-brain barrier disruption, promoting the pathogenesis of vascular cognitive impairment (VCI). In recent years, endothelial cell senescence has emerged as a potential mechanism contributing to microvascular pathologies opening the avenue to the therapeutic exploitation of senolytic drugs in preclinical studies. However, difficulties with the detection of senescent endothelial cells in wild type mouse models of aging hinder the assessment of the efficiency of senolytic treatments. To detect senescent endothelial cells in the aging mouse brain, we analyzed 4233 cells in fractions enriched for cerebromicrovascular endothelial cells and other cells associated with the neurovascular unit obtained from young (3-month-old) and aged (28-month-old) C57BL/6 mice. We define 13 transcriptomic cell types by deep, single-cell RNA sequencing. We match transcriptomic signatures of cellular senescence to endothelial cells identified on the basis of their gene expression profile. Our study demonstrates that with advanced aging, there is an increased ratio of senescent endothelial cells (~ 10%) in the mouse cerebral microcirculation. We propose that our single-cell RNA sequencing-based method can be adapted to study the effect of aging on senescence in various brain cell types as well as to evaluate the efficiency of various senolytic regimens in multiple tissues.
Tárgyszavak:Orvostudományok Elméleti orvostudományok idegen nyelvű folyóiratközlemény külföldi lapban
folyóiratcikk
Aging
Blood-brain barrier
Geroscience
Senescence
Vascular cognitive impairment
Megjelenés:GeroScience. - 42 : 2 (2020), p. 429-444. -
További szerzők:Nyúl-Tóth Ádám Balasubramanian, Priya Tarantini, Stefano Ahire, Chetan DelFavero, Jordan Yabluchanskiy, Andriy Csípő Tamás (1990-) Farkas Eszter Wiley, Graham Garman, Lori Csiszár Anna Ungvári Zoltán
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Intézményi repozitóriumban (DEA) tárolt változat
Borító:
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