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  1. Article ; Online: Personalizing anti-inflammatory therapy in heart failure: A new way.

    Pascual-Figal, Domingo / Fuster, Jose Javier / Bayes-Genis, Antoni

    European journal of heart failure

    2023  Volume 25, Issue 11, Page(s) 1933–1935

    MeSH term(s) Humans ; Heart Failure/drug therapy ; Anti-Inflammatory Agents/therapeutic use
    Chemical Substances Anti-Inflammatory Agents
    Language English
    Publishing date 2023-10-17
    Publishing country England
    Document type Editorial ; Comment
    ZDB-ID 1483672-5
    ISSN 1879-0844 ; 1388-9842
    ISSN (online) 1879-0844
    ISSN 1388-9842
    DOI 10.1002/ejhf.3052
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    In stock of ZB MED Cologne/Königswinter

    Zs.A 5299: Show issues Location:
    Je nach Verfügbarkeit (siehe Angabe bei Bestand)
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    Jg. 1995 - 2021: Lesesall (2.OG)
    ab Jg. 2022: Lesesaal (EG)

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  2. Article: Silencing of microRNA-106b-5p prevents doxorubicin-mediated cardiotoxicity through modulation of the PR55α/YY1/sST2 signaling axis.

    Lax, Antonio / Soler, Fernando / Fernandez Del Palacio, Maria Josefa / Pascual-Oliver, Silvia / Ballester, Miriam Ruiz / Fuster, Jose Javier / Pascual-Figal, Domingo / Asensio-Lopez, Maria Del Carmen

    Molecular therapy. Nucleic acids

    2023  Volume 32, Page(s) 704–720

    Abstract: Clinical use of doxorubicin (Dox), an anthracycline with potent anti-tumor effects, is limited because of its highly chemotherapy-induced cardiotoxicity (CIC). After myocardial infarction (MI), we have recently identified Yin Yang-1 (YY1) and histone ... ...

    Abstract Clinical use of doxorubicin (Dox), an anthracycline with potent anti-tumor effects, is limited because of its highly chemotherapy-induced cardiotoxicity (CIC). After myocardial infarction (MI), we have recently identified Yin Yang-1 (YY1) and histone deacetylase 4 (HDAC4) as two factors involved in the overexpression of the isoform soluble suppression of tumorigenicity 2 (sST2) protein, which acts as a decoy receptor blocking the favorable effects of IL-33. Therefore, high levels of sST2 are associated with increased fibrosis, remodeling, and worse cardiovascular outcomes. No data exist on the role of the YY1/HDAC4/sST2 axis in CIC. This study aimed to evaluate the pathophysiological implication of the molecular YY1/HDAC4/sST2 axis in remodeling that is developed in patients treated with Dox as well as to suggest a novel molecular therapy to prevent anthracycline-induced cardiotoxicity. Here, we have characterized a novel nexus between miR106b-5p (miR-106b) levels and the YY1/HDAC4 axis in relation to the cardiac expression of
    Language English
    Publishing date 2023-05-03
    Publishing country United States
    Document type Journal Article
    ZDB-ID 2662631-7
    ISSN 2162-2531
    ISSN 2162-2531
    DOI 10.1016/j.omtn.2023.04.031
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  3. Article ; Online: Prevalence and characteristics of clonal hematopoiesis in heart failure.

    Palomo, Laura / Santiago-Vacas, Evelyn / Pascual-Figal, Domingo / Fuster, José Javier / Solé, Francesc / Bayés-Genís, Antoni

    Revista espanola de cardiologia (English ed.)

    2021  Volume 74, Issue 11, Page(s) 996–999

    MeSH term(s) Clonal Hematopoiesis ; Heart Failure/epidemiology ; Humans ; Mutation ; Prevalence
    Language Spanish
    Publishing date 2021-06-09
    Publishing country Spain
    Document type Case Reports
    ZDB-ID 2592481-3
    ISSN 1885-5857 ; 1885-5857
    ISSN (online) 1885-5857
    ISSN 1885-5857
    DOI 10.1016/j.rec.2021.05.005
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  4. Article ; Online: Adiponectin attenuates abdominal aortic aneurysm formation in hyperlipidemic mice.

    Yoshida, Sumiko / Fuster, José Javier / Walsh, Kenneth

    Atherosclerosis

    2014  Volume 235, Issue 2, Page(s) 339–346

    Abstract: Objective: Abdominal aortic aneurysms (AAA) are age-associated, life-threatening inflammatory dilations of the abdominal aorta. Human population studies have shown an association between obesity and AAA formation, but the molecular mechanisms underlying ...

    Abstract Objective: Abdominal aortic aneurysms (AAA) are age-associated, life-threatening inflammatory dilations of the abdominal aorta. Human population studies have shown an association between obesity and AAA formation, but the molecular mechanisms underlying this connection remain largely unexplored. Adiponectin is an anti-inflammatory adipokine that is downregulated in obesity. In this study we evaluated the role of adiponectin in a model of AAA using apolipoprotein E/adiponectin double-knockout (Apoe(-/-)Apn(-/-)) mice.
    Approach and results: Angiotensin II (Ang II)-infusion in male Apoe(-/-)Apn(-/-) mice led to a higher incidence of AAA and a significant increase of maximal aortic diameter compared with that of Apoe(-/-) mice (2.12 ± 0.07 mm vs. 1.67 ± 0.09 mm, respectively at 28 days). Adiponectin deficiency augmented the early infiltration of macrophages and increased the expression of pro-inflammatory factors in the dilated aortic wall. MMP-2 and MMP-9 activation was also augmented in the aorta of Apoe(-/-)Apn(-/-) mice compared to Apoe(-/-) mice. These data suggest that the downregulation of adiponectin could directly contribute to the elevated incidence of AAA observed in obese individuals.
    Conclusions: Adiponectin attenuates Ang II-induced vascular inflammation and AAA formation in mice.
    MeSH term(s) Adiponectin/deficiency ; Adiponectin/genetics ; Adiponectin/physiology ; Angiotensin II/pharmacology ; Animals ; Aortic Aneurysm, Abdominal/chemically induced ; Aortic Aneurysm, Abdominal/physiopathology ; Aortic Aneurysm, Abdominal/prevention & control ; Apolipoproteins E/deficiency ; Enzyme Activation ; Macrophages/physiology ; Male ; Matrix Metalloproteinase 2/metabolism ; Matrix Metalloproteinase 9/metabolism ; Mice, Knockout
    Chemical Substances Adiponectin ; Adipoq protein, mouse ; Apolipoproteins E ; Angiotensin II (11128-99-7) ; Matrix Metalloproteinase 2 (EC 3.4.24.24) ; Matrix Metalloproteinase 9 (EC 3.4.24.35)
    Language English
    Publishing date 2014-05-23
    Publishing country Ireland
    Document type Journal Article ; Research Support, N.I.H., Extramural
    ZDB-ID 80061-2
    ISSN 1879-1484 ; 0021-9150
    ISSN (online) 1879-1484
    ISSN 0021-9150
    DOI 10.1016/j.atherosclerosis.2014.05.923
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    Zs.A 226: Show issues Location:
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  5. Article ; Online: A role for miR-33 in p53 regulation: New perspectives for hematopoietic stem cell research.

    Fuster, José Javier / Andrés, Vicente

    Cell cycle (Georgetown, Tex.)

    2010  Volume 9, Issue 17, Page(s) 3397–3398

    MeSH term(s) 3' Untranslated Regions ; Animals ; Cell Line, Tumor ; Down-Regulation ; Hematopoietic Stem Cells/cytology ; Hematopoietic Stem Cells/metabolism ; Humans ; Mice ; MicroRNAs/metabolism ; Signal Transduction ; Tumor Suppressor Protein p53/genetics ; Tumor Suppressor Protein p53/metabolism
    Chemical Substances 3' Untranslated Regions ; MicroRNAs ; Mirn33 microRNA, mouse ; Tumor Suppressor Protein p53
    Language English
    Publishing date 2010-09-22
    Publishing country United States
    Document type Comment ; News ; Research Support, Non-U.S. Gov't
    ZDB-ID 2146183-1
    ISSN 1551-4005 ; 1538-4101 ; 1554-8627
    ISSN (online) 1551-4005
    ISSN 1538-4101 ; 1554-8627
    DOI 10.4161/cc.9.17.13070
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    Zs.A 5881: Show issues Location:
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  6. Article ; Online: Subclinical atherosclerosis and accelerated epigenetic age mediated by inflammation: a multi-omics study.

    Sánchez-Cabo, Fátima / Fuster, Valentín / Silla-Castro, Juan Carlos / González, Gema / Lorenzo-Vivas, Erika / Alvarez, Rebeca / Callejas, Sergio / Benguría, Alberto / Gil, Eduardo / Núñez, Estefanía / Oliva, Belén / Mendiguren, José María / Cortes-Canteli, Marta / Bueno, Héctor / Andrés, Vicente / Ordovás, Jose María / Fernández-Friera, Leticia / Quesada, Antonio J / Garcia, Jose Manuel /
    Rossello, Xavier / Vázquez, Jesús / Dopazo, Ana / Fernández-Ortiz, Antonio / Ibáñez, Borja / Fuster, Jose Javier / Lara-Pezzi, Enrique

    European heart journal

    2023  Volume 44, Issue 29, Page(s) 2698–2709

    Abstract: Aims: Epigenetic age is emerging as a personalized and accurate predictor of biological age. The aim of this article is to assess the association of subclinical atherosclerosis with accelerated epigenetic age and to investigate the underlying mechanisms ...

    Abstract Aims: Epigenetic age is emerging as a personalized and accurate predictor of biological age. The aim of this article is to assess the association of subclinical atherosclerosis with accelerated epigenetic age and to investigate the underlying mechanisms mediating this association.
    Methods and results: Whole blood methylomics, transcriptomics, and plasma proteomics were obtained for 391 participants of the Progression of Early Subclinical Atherosclerosis study. Epigenetic age was calculated from methylomics data for each participant. Its divergence from chronological age is termed epigenetic age acceleration. Subclinical atherosclerosis burden was estimated by multi-territory 2D/3D vascular ultrasound and by coronary artery calcification. In healthy individuals, the presence, extension, and progression of subclinical atherosclerosis were associated with a significant acceleration of the Grim epigenetic age, a predictor of health and lifespan, regardless of traditional cardiovascular risk factors. Individuals with an accelerated Grim epigenetic age were characterized by an increased systemic inflammation and associated with a score of low-grade, chronic inflammation. Mediation analysis using transcriptomics and proteomics data revealed key pro-inflammatory pathways (IL6, Inflammasome, and IL10) and genes (IL1B, OSM, TLR5, and CD14) mediating the association between subclinical atherosclerosis and epigenetic age acceleration.
    Conclusion: The presence, extension, and progression of subclinical atherosclerosis in middle-aged asymptomatic individuals are associated with an acceleration in the Grim epigenetic age. Mediation analysis using transcriptomics and proteomics data suggests a key role of systemic inflammation in this association, reinforcing the relevance of interventions on inflammation to prevent cardiovascular disease.
    MeSH term(s) Middle Aged ; Humans ; Multiomics ; Atherosclerosis/genetics ; Coronary Artery Disease ; Inflammation/genetics ; Epigenesis, Genetic ; Risk Factors
    Language English
    Publishing date 2023-06-20
    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/ehad361
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    Zs.A 1563: Show issues Location:
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    Jg. 1995 - 2021: Lesesall (1.OG)
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    Zs.MO 640: Show issues

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  7. Article ; Online: An antiangiogenic isoform of VEGF-A contributes to impaired vascularization in peripheral artery disease.

    Kikuchi, Ryosuke / Nakamura, Kazuto / MacLauchlan, Susan / Ngo, Doan Thi-Minh / Shimizu, Ippei / Fuster, Jose Javier / Katanasaka, Yasufumi / Yoshida, Sumiko / Qiu, Yan / Yamaguchi, Terry P / Matsushita, Tadashi / Murohara, Toyoaki / Gokce, Noyan / Bates, David O / Hamburg, Naomi M / Walsh, Kenneth

    Nature medicine

    2014  Volume 20, Issue 12, Page(s) 1464–1471

    Abstract: Peripheral artery disease (PAD) generates tissue ischemia through arterial occlusions and insufficient collateral vessel formation. Vascular insufficiency in PAD occurs despite higher circulating levels of vascular endothelial growth factor A (VEGF-A), a ...

    Abstract Peripheral artery disease (PAD) generates tissue ischemia through arterial occlusions and insufficient collateral vessel formation. Vascular insufficiency in PAD occurs despite higher circulating levels of vascular endothelial growth factor A (VEGF-A), a key regulator of angiogenesis. Here we show that clinical PAD is associated with elevated levels of an antiangiogenic VEGF-A splice isoform (VEGF-A165b) and a corresponding reduction in levels of the proangiogenic VEGF-A165a splice isoform. In mice, VEGF-A165b expression was upregulated by conditions associated with impaired limb revascularization, including leptin deficiency, diet-induced obesity, genetic ablation of the secreted frizzled-related protein 5 (Sfrp5) adipokine and transgenic overexpression of Wnt5a in myeloid cells. In a mouse model of PAD, delivery of VEGF-A165b inhibited revascularization of ischemic hind limbs, whereas treatment with an isoform-specific neutralizing antibody reversed impaired revascularization caused by metabolic dysfunction or perturbations in the Wnt5a-Sfrp5 regulatory system. These results indicate that inflammation-driven expression of the antiangiogenic VEGF-A isoform can contribute to impaired collateralization in ischemic cardiovascular disease.
    MeSH term(s) Adaptor Proteins, Signal Transducing ; Animals ; Collateral Circulation ; Disease Models, Animal ; Humans ; Intercellular Signaling Peptides and Proteins/genetics ; Mice ; Mice, Knockout ; Mice, Transgenic ; Neovascularization, Physiologic/physiology ; Peripheral Arterial Disease/metabolism ; Protein Isoforms ; Vascular Endothelial Growth Factor A/metabolism ; Wnt Proteins/genetics ; Wnt-5a Protein
    Chemical Substances Adaptor Proteins, Signal Transducing ; Intercellular Signaling Peptides and Proteins ; Protein Isoforms ; Sfrp5 protein, mouse ; Vascular Endothelial Growth Factor A ; Wnt Proteins ; Wnt-5a Protein ; Wnt5a protein, mouse
    Language English
    Publishing date 2014-11-02
    Publishing country United States
    Document type Journal Article ; Research Support, N.I.H., Extramural ; Research Support, Non-U.S. Gov't
    ZDB-ID 1220066-9
    ISSN 1546-170X ; 1078-8956
    ISSN (online) 1546-170X
    ISSN 1078-8956
    DOI 10.1038/nm.3703
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