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Article ; Online: The curious case of dermal fibroblasts: cell identity loss may be a mechanism underlying cardiovascular aging.

Badi, Ileana

2019 Volume 115, Issue 3, Page(s) e24–e25

MeSH term(s)	Adipogenesis ; Fibroblasts ; Skin Aging
Language	English
Publishing date	2019-02-12
Publishing country	England
Document type	Journal Article ; Research Support, Non-U.S. Gov't ; Comment
ZDB-ID	80340-6
ISSN	1755-3245 ; 0008-6363
ISSN (online)	1755-3245
ISSN	0008-6363
DOI	10.1093/cvr/cvz012
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Article ; Online: Brown Adipose Tissue and the Take (12,13-di)HOME Message to the Heart.

Badi, Ileana / Antoniades, Charalambos

Circulation

2021 Volume 143, Issue 2, Page(s) 160–162

MeSH term(s)	Adipose Tissue, Brown ; Heart ; Humans ; Myocardium
Language	English
Publishing date	2021-01-11
Publishing country	United States
Document type	Editorial ; Research Support, Non-U.S. Gov't ; Comment
ZDB-ID	80099-5
ISSN	1524-4539 ; 0009-7322 ; 0069-4193 ; 0065-8499
ISSN (online)	1524-4539
ISSN	0009-7322 ; 0069-4193 ; 0065-8499
DOI	10.1161/CIRCULATIONAHA.120.051981
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Article: Editorial: Exploring the Crosstalk Between Adipose Tissue and the Cardiovascular System.

Badi, Ileana / Sommariva, Elena / Miyazawa, Kazuo / Kondo, Hidekazu / Azzimato, Valerio / Akawi, Nadia

Frontiers in cell and developmental biology

2022 Volume 10, Page(s) 973135

Language	English
Publishing date	2022-07-15
Publishing country	Switzerland
Document type	Editorial
ZDB-ID	2737824-X
ISSN	2296-634X
ISSN	2296-634X
DOI	10.3389/fcell.2022.973135
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Article ; Online: MicroRNA-34a: the bad guy in age-related vascular diseases

Raucci, Angela / Macrì, Federica / Castiglione, Stefania / Badi, Ileana / Vinci, Maria Cristina / Zuccolo, Estella

Cell. Mol. Life Sci.. 2021 Dec., v. 78, no. 23 p.7355-7378

2021

Abstract: The age-related vasculature alteration is the prominent risk factor for vascular diseases (VD), namely, atherosclerosis, abdominal aortic aneurysm, vascular calcification (VC) and pulmonary arterial hypertension (PAH). The chronic sterile low-grade ... ...

Abstract	The age-related vasculature alteration is the prominent risk factor for vascular diseases (VD), namely, atherosclerosis, abdominal aortic aneurysm, vascular calcification (VC) and pulmonary arterial hypertension (PAH). The chronic sterile low-grade inflammation state, alias inflammaging, characterizes elderly people and participates in VD development. MicroRNA34-a (miR-34a) is emerging as an important mediator of inflammaging and VD. miR-34a increases with aging in vessels and induces senescence and the acquisition of the senescence-associated secretory phenotype (SASP) in vascular smooth muscle (VSMCs) and endothelial (ECs) cells. Similarly, other VD risk factors, including dyslipidemia, hyperglycemia and hypertension, modify miR-34a expression to promote vascular senescence and inflammation. miR-34a upregulation causes endothelial dysfunction by affecting ECs nitric oxide bioavailability, adhesion molecules expression and inflammatory cells recruitment. miR-34a-induced senescence facilitates VSMCs osteoblastic switch and VC development in hyperphosphatemia conditions. Conversely, atherogenic and hypoxic stimuli downregulate miR-34a levels and promote VSMCs proliferation and migration during atherosclerosis and PAH. MiR34a genetic ablation or miR-34a inhibition by anti-miR-34a molecules in different experimental models of VD reduce vascular inflammation, senescence and apoptosis through sirtuin 1 Notch1, and B-cell lymphoma 2 modulation. Notably, pleiotropic drugs, like statins, liraglutide and metformin, affect miR-34a expression. Finally, human studies report that miR-34a levels associate to atherosclerosis and diabetes and correlate with inflammatory factors during aging. Herein, we comprehensively review the current knowledge about miR-34a-dependent molecular and cellular mechanisms activated by VD risk factors and highlight the diagnostic and therapeutic potential of modulating its expression in order to reduce inflammaging and VD burn and extend healthy lifespan.
Keywords	B-cell lymphoma ; adhesion ; aneurysm ; apoptosis ; atherosclerosis ; bioavailability ; calcification ; diabetes ; elderly ; humans ; hyperglycemia ; hyperlipidemia ; hypertension ; inflammation ; longevity ; metformin ; nitric oxide ; people ; phenotype ; pulmonary artery ; risk factors ; sirtuins ; smooth muscle ; therapeutics
Language	English
Dates of publication	2021-12
Size	p. 7355-7378.
Publishing place	Springer International Publishing
Document type	Article ; Online
Note	Review
ZDB-ID	1358415-7
ISSN	1420-9071 ; 1420-682X
ISSN (online)	1420-9071
ISSN	1420-682X
DOI	10.1007/s00018-021-03979-4
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Article ; Online: MicroRNA-34a: the bad guy in age-related vascular diseases.

Raucci, Angela / Macrì, Federica / Castiglione, Stefania / Badi, Ileana / Vinci, Maria Cristina / Zuccolo, Estella

Cellular and molecular life sciences : CMLS

2021 Volume 78, Issue 23, Page(s) 7355–7378

Abstract	The age-related vasculature alteration is the prominent risk factor for vascular diseases (VD), namely, atherosclerosis, abdominal aortic aneurysm, vascular calcification (VC) and pulmonary arterial hypertension (PAH). The chronic sterile low-grade inflammation state, alias inflammaging, characterizes elderly people and participates in VD development. MicroRNA34-a (miR-34a) is emerging as an important mediator of inflammaging and VD. miR-34a increases with aging in vessels and induces senescence and the acquisition of the senescence-associated secretory phenotype (SASP) in vascular smooth muscle (VSMCs) and endothelial (ECs) cells. Similarly, other VD risk factors, including dyslipidemia, hyperglycemia and hypertension, modify miR-34a expression to promote vascular senescence and inflammation. miR-34a upregulation causes endothelial dysfunction by affecting ECs nitric oxide bioavailability, adhesion molecules expression and inflammatory cells recruitment. miR-34a-induced senescence facilitates VSMCs osteoblastic switch and VC development in hyperphosphatemia conditions. Conversely, atherogenic and hypoxic stimuli downregulate miR-34a levels and promote VSMCs proliferation and migration during atherosclerosis and PAH. MiR34a genetic ablation or miR-34a inhibition by anti-miR-34a molecules in different experimental models of VD reduce vascular inflammation, senescence and apoptosis through sirtuin 1 Notch1, and B-cell lymphoma 2 modulation. Notably, pleiotropic drugs, like statins, liraglutide and metformin, affect miR-34a expression. Finally, human studies report that miR-34a levels associate to atherosclerosis and diabetes and correlate with inflammatory factors during aging. Herein, we comprehensively review the current knowledge about miR-34a-dependent molecular and cellular mechanisms activated by VD risk factors and highlight the diagnostic and therapeutic potential of modulating its expression in order to reduce inflammaging and VD burn and extend healthy lifespan.
MeSH term(s)	Aortic Aneurysm, Abdominal/genetics ; Aortic Aneurysm, Abdominal/pathology ; Atherosclerosis/genetics ; Atherosclerosis/pathology ; Cardiovascular Diseases/genetics ; Cardiovascular Diseases/pathology ; Cardiovascular System/pathology ; Cellular Senescence/physiology ; Endothelial Cells/metabolism ; Humans ; Inflammation/genetics ; Inflammation/pathology ; MicroRNAs/genetics ; Muscle, Smooth, Vascular/pathology ; Pulmonary Arterial Hypertension/genetics ; Pulmonary Arterial Hypertension/pathology ; Vascular Calcification/genetics ; Vascular Calcification/pathology
Chemical Substances	MIRN34 microRNA, human ; MicroRNAs
Language	English
Publishing date	2021-10-26
Publishing country	Switzerland
Document type	Journal Article ; Review
ZDB-ID	1358415-7
ISSN	1420-9071 ; 1420-682X
ISSN (online)	1420-9071
ISSN	1420-682X
DOI	10.1007/s00018-021-03979-4
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Article ; Online: Role of Human Epicardial Adipose Tissue-Derived miR-92a-3p in Myocardial Redox State.

Carena, Maria Cristina / Badi, Ileana / Polkinghorne, Murray / Akoumianakis, Ioannis / Psarros, Costas / Wahome, Elizabeth / Kotanidis, Christos P / Akawi, Nadia / Antonopoulos, Alexios S / Chauhan, Jagat / Sayeed, Rana / Krasopoulos, George / Srivastava, Vivek / Farid, Shakil / Walcot, Nicholas / Douglas, Gillian / Channon, Keith M / Casadei, Barbara / Antoniades, Charalambos

Journal of the American College of Cardiology

2023 Volume 82, Issue 4, Page(s) 317–332

Abstract: Background: Visceral obesity is directly linked to increased cardiovascular risk, including heart failure.: Objectives: This study explored the ability of human epicardial adipose tissue (EAT)-derived microRNAs (miRNAs) to regulate the myocardial ... ...

Abstract	Background: Visceral obesity is directly linked to increased cardiovascular risk, including heart failure. Objectives: This study explored the ability of human epicardial adipose tissue (EAT)-derived microRNAs (miRNAs) to regulate the myocardial redox state and clinical outcomes. Methods: This study screened for miRNAs expressed and released from human EAT and tested for correlations with the redox state in the adjacent myocardium in paired EAT/atrial biopsy specimens from patients undergoing cardiac surgery. Three miRNAs were then tested for causality in an in vitro model of cardiomyocytes. At a clinical level, causality/directionality were tested using genome-wide association screening, and the underlying mechanisms were explored using human biopsy specimens, as well as overexpression of the candidate miRNAs and their targets in vitro and in vivo using a transgenic mouse model. The final prognostic value of the discovered targets was tested in patients undergoing cardiac surgery, followed up for a median of 8 years. Results: EAT miR-92a-3p was related to lower oxidative stress in human myocardium, a finding confirmed by using genetic regulators of miR-92a-3p in the human heart and EAT. miR-92a-3p reduced nicotinamide adenine dinucleotide phosphate (NADPH)-oxidase-derived superoxide (O Conclusions: EAT-derived miRNAs exert paracrine effects on the human heart. Indeed miR-92a-3p suppresses the wingless-type MMTV integration site family, member 5a/Rac1/NADPH oxidase axis and improves the myocardial redox state. EAT-derived miR-92a-3p is related to improved clinical outcomes and is a rational therapeutic target for the prevention and treatment of obesity-related heart disease.
MeSH term(s)	Humans ; Mice ; Animals ; Genome-Wide Association Study ; MicroRNAs/genetics ; MicroRNAs/metabolism ; Myocardium/metabolism ; Oxidation-Reduction ; Mice, Transgenic ; Adipose Tissue/metabolism
Chemical Substances	MicroRNAs
Language	English
Publishing date	2023-07-19
Publishing country	United States
Document type	Journal Article ; Research Support, Non-U.S. Gov't
ZDB-ID	605507-2
ISSN	1558-3597 ; 0735-1097
ISSN (online)	1558-3597
ISSN	0735-1097
DOI	10.1016/j.jacc.2023.05.031
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Zs.A 1846: Show issues			Location: Je nach Verfügbarkeit (siehe Angabe bei Bestand) bis Jg. 1994: Bestellungen von Artikeln über das Online-Bestellformular Jg. 1995 - 2021: Lesesall (1.OG) ab Jg. 2022: Lesesaal (EG)
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Article ; Online: The microRNA-34a-Induced Senescence-Associated Secretory Phenotype (SASP) Favors Vascular Smooth Muscle Cells Calcification.

Zuccolo, Estella / Badi, Ileana / Scavello, Francesco / Gambuzza, Irene / Mancinelli, Luigi / Macrì, Federica / Tedesco, Calogero C / Veglia, Fabrizio / Bonfigli, Anna Rita / Olivieri, Fabiola / Raucci, Angela

International journal of molecular sciences

2020 Volume 21, Issue 12

Abstract: The senescence of vascular smooth muscle cells (VSMCs), characterized by the acquisition of senescence-associated secretory phenotype (SASP), is relevant for VSMCs osteoblastic differentiation and vascular calcification (VC). MicroRNA-34a (miR-34a) is a ... ...

Abstract	The senescence of vascular smooth muscle cells (VSMCs), characterized by the acquisition of senescence-associated secretory phenotype (SASP), is relevant for VSMCs osteoblastic differentiation and vascular calcification (VC). MicroRNA-34a (miR-34a) is a driver of such phenomena and could play a role in vascular inflammaging. Herein, we analyzed the relationship between miR-34a and the prototypical SASP component IL6 in in vitro and in vivo models. miR-34a and IL6 levels increased and positively correlated in aortas of 21 months-old male C57BL/6J mice and in human aortic smooth muscle cells (HASMCs) isolated from donors of different age and undergone senescence. Lentiviral overexpression of miR-34a in HASMCs enhanced IL6 secretion. HASMCs senescence and calcification accelerated after exposure to conditioned medium of miR-34a-overexpressing cells. Analysis of miR-34a-induced secretome revealed enhancement of several pro-inflammatory cytokines and chemokines, including IL6, pro-senescent growth factors and matrix-degrading molecules. Moreover, induction of aortas medial calcification and concomitant IL6 expression, with an overdose of vitamin D, was reduced in male C57BL/6J
MeSH term(s)	Adult ; Aged ; Aged, 80 and over ; Animals ; Cell Differentiation ; Cell Proliferation ; Cells, Cultured ; Cellular Senescence ; Female ; Healthy Volunteers ; Humans ; Interleukin-6/genetics ; Interleukin-6/metabolism ; Male ; Mice ; Mice, Inbred C57BL ; MicroRNAs/genetics ; Middle Aged ; Muscle, Smooth, Vascular/metabolism ; Muscle, Smooth, Vascular/pathology ; Vascular Calcification/genetics ; Vascular Calcification/metabolism ; Vascular Calcification/pathology ; Young Adult
Chemical Substances	Interleukin-6 ; MIRN34 microRNA, human ; MIRN34a microRNA, mouse ; MicroRNAs
Language	English
Publishing date	2020-06-23
Publishing country	Switzerland
Document type	Journal Article
ZDB-ID	2019364-6
ISSN	1422-0067 ; 1422-0067 ; 1661-6596
ISSN (online)	1422-0067
ISSN	1422-0067 ; 1661-6596
DOI	10.3390/ijms21124454
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Article ; Online: Effects of canagliflozin on human myocardial redox signalling: clinical implications.

European heart journal

2021 Volume 42, Issue 48, Page(s) 4947–4960

Abstract: Aims: Recent clinical trials indicate that sodium-glucose cotransporter 2 (SGLT2) inhibitors improve cardiovascular outcomes in heart failure patients, but the underlying mechanisms remain unknown. We explored the direct effects of canagliflozin, an ... ...

Abstract	Aims: Recent clinical trials indicate that sodium-glucose cotransporter 2 (SGLT2) inhibitors improve cardiovascular outcomes in heart failure patients, but the underlying mechanisms remain unknown. We explored the direct effects of canagliflozin, an SGLT2 inhibitor with mild SGLT1 inhibitory effects, on myocardial redox signalling in humans. Methods and results: Study 1 included 364 patients undergoing cardiac surgery. Right atrial appendage biopsies were harvested to quantify superoxide (O2.-) sources and the expression of inflammation, fibrosis, and myocardial stretch genes. In Study 2, atrial tissue from 51 patients was used ex vivo to study the direct effects of canagliflozin on NADPH oxidase activity and nitric oxide synthase (NOS) uncoupling. Differentiated H9C2 and primary human cardiomyocytes (hCM) were used to further characterize the underlying mechanisms (Study 3). SGLT1 was abundantly expressed in human atrial tissue and hCM, contrary to SGLT2. Myocardial SGLT1 expression was positively associated with O2.- production and pro-fibrotic, pro-inflammatory, and wall stretch gene expression. Canagliflozin reduced NADPH oxidase activity via AMP kinase (AMPK)/Rac1signalling and improved NOS coupling via increased tetrahydrobiopterin bioavailability ex vivo and in vitro. These were attenuated by knocking down SGLT1 in hCM. Canagliflozin had striking ex vivo transcriptomic effects on myocardial redox signalling, suppressing apoptotic and inflammatory pathways in hCM. Conclusions: We demonstrate for the first time that canagliflozin suppresses myocardial NADPH oxidase activity and improves NOS coupling via SGLT1/AMPK/Rac1 signalling, leading to global anti-inflammatory and anti-apoptotic effects in the human myocardium. These findings reveal a novel mechanism contributing to the beneficial cardiac effects of canagliflozin.
MeSH term(s)	Canagliflozin/metabolism ; Canagliflozin/pharmacology ; Humans ; Myocardium ; Myocytes, Cardiac/metabolism ; Oxidation-Reduction ; Sodium-Glucose Transporter 2 Inhibitors/pharmacology
Chemical Substances	Sodium-Glucose Transporter 2 Inhibitors ; Canagliflozin (0SAC974Z85)
Language	English
Publishing date	2021-07-16
Publishing country	England
Document type	Journal Article ; Research Support, Non-U.S. Gov't
ZDB-ID	603098-1
ISSN	1522-9645 ; 0195-668X
ISSN (online)	1522-9645
ISSN	0195-668X
DOI	10.1093/eurheartj/ehab420
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Zs.A 1563: Show issues			Location: Je nach Verfügbarkeit (siehe Angabe bei Bestand) bis Jg. 1994: Bestellungen von Artikeln über das Online-Bestellformular Jg. 1995 - 2021: Lesesall (1.OG) ab Jg. 2022: Lesesaal (EG)
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Article ; Online: Fat-Secreted Ceramides Regulate Vascular Redox State and Influence Outcomes in Patients With Cardiovascular Disease.

Journal of the American College of Cardiology

2021 Volume 77, Issue 20, Page(s) 2494–2513

Abstract: Background: Obesity is associated with increased cardiovascular risk; however, the potential role of dysregulations in the adipose tissue (AT) metabolome is unknown.: Objectives: The aim of this study was to explore the role of dysregulation in the ... ...

Abstract	Background: Obesity is associated with increased cardiovascular risk; however, the potential role of dysregulations in the adipose tissue (AT) metabolome is unknown. Objectives: The aim of this study was to explore the role of dysregulation in the AT metabolome on vascular redox signaling and cardiovascular outcomes. Methods: A screen was conducted for metabolites differentially secreted by thoracic AT (ThAT) and subcutaneous AT in obese patients with atherosclerosis (n = 48), and these metabolites were then linked with dysregulated vascular redox signaling in 633 patients undergoing coronary bypass surgery. The underlying mechanisms were explored in human aortic endothelial cells, and their clinical value was tested against hard clinical endpoints. Results: Because ThAT volume was associated significantly with arterial oxidative stress, there were significant differences in sphingolipid secretion between ThAT and subcutaneous AT, with C16:0-ceramide and derivatives being the most abundant species released within adipocyte-derived extracellular vesicles. High ThAT sphingolipid secretion was significantly associated with reduced endothelial nitric oxide bioavailability and increased superoxide generated in human vessels. Circulating C16:0-ceramide correlated positively with ThAT ceramides, dysregulated vascular redox signaling, and increased systemic inflammation in 633 patients with atherosclerosis. Exogenous C16:0-ceramide directly increased superoxide via tetrahydrobiopterin-mediated endothelial nitric oxide synthase uncoupling and dysregulated protein phosphatase 2 in human aortic endothelial cells. High plasma C16:0-ceramide and its glycosylated derivative were independently related with increased risk for cardiac mortality (adjusted hazard ratios: 1.394; 95% confidence interval: 1.030 to 1.886; p = 0.031 for C16:0-ceramide and 1.595; 95% confidence interval: 1.042 to 2.442; p = 0.032 for C16:0-glycosylceramide per 1 SD). In a randomized controlled clinical trial, 1-year treatment of obese patients with the glucagon-like peptide-1 analog liraglutide suppressed plasma C16:0-ceramide and C16:0-glycosylceramide changes compared with control subjects. Conclusions: These results demonstrate for the first time in humans that AT-derived ceramides are modifiable regulators of vascular redox state in obesity, with a direct impact on cardiac mortality in advanced atherosclerosis. (The Interaction Between Appetite Hormones; NCT02094183).
MeSH term(s)	Adipose Tissue/metabolism ; Arteries/metabolism ; Atherosclerosis/complications ; Atherosclerosis/metabolism ; Atherosclerosis/mortality ; Case-Control Studies ; Ceramides/metabolism ; Endothelium, Vascular/metabolism ; Extracellular Vesicles/metabolism ; Humans ; In Vitro Techniques ; Liraglutide ; Metabolomics ; Obesity/complications ; Obesity/metabolism ; Oxidative Stress ; Randomized Controlled Trials as Topic ; Sphingolipids/metabolism ; Superoxides/metabolism
Chemical Substances	Ceramides ; Sphingolipids ; Superoxides (11062-77-4) ; Liraglutide (839I73S42A)
Language	English
Publishing date	2021-05-20
Publishing country	United States
Document type	Journal Article ; Research Support, Non-U.S. Gov't
ZDB-ID	605507-2
ISSN	1558-3597 ; 0735-1097
ISSN (online)	1558-3597
ISSN	0735-1097
DOI	10.1016/j.jacc.2021.03.314
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Article ; Online: miR-34a Promotes Vascular Smooth Muscle Cell Calcification by Downregulating SIRT1 (Sirtuin 1) and Axl (AXL Receptor Tyrosine Kinase).

Badi, Ileana / Mancinelli, Luigi / Polizzotto, Andrea / Ferri, Debora / Zeni, Filippo / Burba, Ilaria / Milano, Giuseppina / Brambilla, Francesca / Saccu, Claudio / Bianchi, Marco E / Pompilio, Giulio / Capogrossi, Maurizio C / Raucci, Angela

Arteriosclerosis, thrombosis, and vascular biology

2018 Volume 38, Issue 9, Page(s) 2079–2090

Abstract: Objective- Vascular calcification (VC) is age dependent and a risk factor for cardiovascular and all-cause mortality. VC involves the senescence-induced transdifferentiation of vascular smooth muscle cells (SMCs) toward an osteochondrogenic lineage ... ...

Abstract	Objective- Vascular calcification (VC) is age dependent and a risk factor for cardiovascular and all-cause mortality. VC involves the senescence-induced transdifferentiation of vascular smooth muscle cells (SMCs) toward an osteochondrogenic lineage resulting in arterial wall mineralization. miR-34a increases with age in aortas and induces vascular SMC senescence through the modulation of its target SIRT1 (sirtuin 1). In this study, we aimed to investigate whether miR-34a regulates VC. Approach and Results- We found that miR-34a and Runx2 (Runt-related transcription factor 2) expression correlates in young and old mice. Mir34a
MeSH term(s)	Adult ; Aging/pathology ; Animals ; Aorta/metabolism ; Cell Proliferation ; Cells, Cultured ; Cellular Senescence/physiology ; Core Binding Factor Alpha 1 Subunit/metabolism ; Down-Regulation ; Humans ; Male ; Mice ; Mice, Knockout ; MicroRNAs/metabolism ; Muscle, Smooth, Vascular/cytology ; Muscle, Smooth, Vascular/metabolism ; Myocytes, Smooth Muscle/metabolism ; Proto-Oncogene Proteins/metabolism ; Receptor Protein-Tyrosine Kinases/metabolism ; SOX9 Transcription Factor/metabolism ; Sirtuin 1/metabolism ; Up-Regulation ; Vascular Calcification ; Young Adult
Chemical Substances	Core Binding Factor Alpha 1 Subunit ; MIRN34a microRNA, mouse ; MicroRNAs ; Proto-Oncogene Proteins ; Runx2 protein, mouse ; SOX9 Transcription Factor ; Sox9 protein, mouse ; Receptor Protein-Tyrosine Kinases (EC 2.7.10.1) ; axl receptor tyrosine kinase (EC 2.7.10.1) ; Sirt1 protein, mouse (EC 3.5.1.-) ; Sirtuin 1 (EC 3.5.1.-)
Language	English
Publishing date	2018-07-18
Publishing country	United States
Document type	Journal Article ; Research Support, Non-U.S. Gov't
ZDB-ID	1221433-4
ISSN	1524-4636 ; 1079-5642
ISSN (online)	1524-4636
ISSN	1079-5642
DOI	10.1161/ATVBAHA.118.311298
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