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Ornella Colpani IRCCS MultiMedica, Milan, Italy

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Gaia Spinetti IRCCS MultiMedica, Milan, Italy

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). Excessive extracellular or intracellular stress triggers cellular senescence (CS) in proliferation-competent cells inducing growth arrest and failure to re-enter the cell division cycle. In addition to durable growth arrest, senescent cells show high SAβ

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Ka Ka Ting Centre for the Endothelium Vascular Biology Program Centenary Institute, The University of Sydney, Sydney, New South Wales, Australia

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Paul Coleman Centre for the Endothelium Vascular Biology Program Centenary Institute, The University of Sydney, Sydney, New South Wales, Australia

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Yang Zhao Centre for the Endothelium Vascular Biology Program Centenary Institute, The University of Sydney, Sydney, New South Wales, Australia

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Mathew A Vadas Centre for the Endothelium Vascular Biology Program Centenary Institute, The University of Sydney, Sydney, New South Wales, Australia

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Jennifer R Gamble Centre for the Endothelium Vascular Biology Program Centenary Institute, The University of Sydney, Sydney, New South Wales, Australia

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indeed endothelial dysfunctions including arterial stiffening ( 6 ), impaired neovascularization ( 7 ) and loss of tissue-barrier function are evident in age-related diseases ( 8 ). This review will focus on cellular aging or senescence of the vascular

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Amer Harky Department of Cardiothoracic Surgery, Liverpool Heart and Chest, Liverpool, UK

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Ka Siu Fan St. George’s Medical School, University of London, London, UK

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Ka Hay Fan Faculty of Medicine, Imperial College London, London, UK

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-surgical management and preventative action can further reduce the burden of TAAD on our society. Of the 5160 deaths in the United Kingdom attributed to aortic aneurysms and dissections in 2017, the majority occurred in the elderly: with the rise of senescence, it is

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Alessandra Magenta Istituto Dermopatico dell’Immacolata, IDI-IRCCS, Rome, Italy

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Reggio Lorde Bristol Medical School (Translational Health Sciences), Bristol Heart Institute, University of Bristol, Bristol, UK

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Sunayana Begum Syed Laboratory of Cardiovascular Science, National Institute on Aging, National Institutes of Health, Baltimore, Maryland, USA

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Maurizio C Capogrossi Laboratory of Cardiovascular Science, National Institute on Aging, National Institutes of Health, Baltimore, Maryland, USA
Division of Cardiology, Johns Hopkins Bayview Medical Center, Baltimore, Maryland, USA

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Annibale Puca Ageing Unit, IRCCS MultiMedica, Milan, Italy
Department of Medicine, Surgery and Dentistry, ‘Scuola Medica Salernitana’ University of Salerno, Baronissi, Italy

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Paolo Madeddu Bristol Medical School (Translational Health Sciences), Bristol Heart Institute, University of Bristol, Bristol, UK

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oxidative stress, mitochondrial dysfunction, susceptibility to molecular stressors, chronic low-grade inflammation, genomic instability, cellular senescence, epigenetic alterations, loss of proteostasis, deregulated nutrient sensing, and stem cell

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Sarah Costantino Center for Molecular Cardiology, University of Zürich, Zürich, Switzerland

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Shafeeq A Mohammed Center for Molecular Cardiology, University of Zürich, Zürich, Switzerland

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Samuele Ambrosini Center for Molecular Cardiology, University of Zürich, Zürich, Switzerland

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Francesco Paneni Center for Molecular Cardiology, University of Zürich, Zürich, Switzerland
University Heart Center, Cardiology, University Hospital Zurich, Zürich, Switzerland
Department of Research and Education, University Hospital Zurich, Zürich, Switzerland

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Our genetic background provides limited information on individual risk of developing vascular complications overtime. New biological layers, namely epigenetic modifications, are now emerging as potent regulators of gene expression thus leading to altered transcriptional programs and vascular disease phenotypes. Such epigenetic modifications, defined as changes to the genome that do not involve changes in DNA sequence, are generally induced by environmental factors and poor lifestyle habits. Of note, adverse epigenetic signals acquired during life can be transmitted to the offspring thus leading to premature alterations of the epigenetic and transcriptional landscape eventually leading to early endothelial dysfunction and vascular senescence. Modifications of the epigenome play a pivotal role in the pathophysiology of cardiometabolic disturbances such as obesity and type 2 diabetes. In these patients, changes of DNA methylation and chromatin structure contribute to alter pathways regulating insulin sensitivity, glucose homeostasis, adipogenesis and vascular function. In this perspective, unveiling the ‘epigenetic landscape’ in cardiometabolic patients may help to identify new players implicated in obesity and diabetes-related vascular dysfunction and may pave the way for personalized therapies in this setting. In the present review, we discuss current knowledge of the epigenetic routes implicated in vascular damage and cardiovascular disease in patients with metabolic alterations.

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Vladimir Y Bogdanov Division of Hematology/Oncology, Department of Internal Medicine, University of Cincinnati College of Medicine, Cincinnati, Ohio, USA

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Vladimir N Khirmanov Department of Cardiovascular Medicine, Nikiforov’s All-Russian Center for Emergency and Radiation Medicine, Saint Petersburg, Russia

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hyperactivated in patients with long COVID ( 64 ), which may explain the fact that d-dimer levels can remain elevated up to several months post-acute phase of the disease ( 65 ). Virus-induced cellular senescence may be of particular relevance to platelet

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Maria Luigia Carbone Experimental Immunology Laboratory, IDI-IRCCS, Rome, Italy

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Cristina Maria Failla Experimental Immunology Laboratory, IDI-IRCCS, Rome, Italy

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senescence-associated secretory phenotype (SASP), activated by senescent cells ( 10 ). Diverse ILs are present in the SASP, mainly IL1A, IL1, IL6, and IL8 ( 11 ), and they can act on ECs in an autocrine, when secreted by senescent ECs themselves, or in a

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Sara Sileno Istituto Dermopatico dell’Immacolata, IDI-IRCCS, Experimental Immunology Laboratory Via Monti di Creta, Rome, Italy

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Sara Beji Istituto Dermopatico dell’Immacolata, IDI-IRCCS, Experimental Immunology Laboratory Via Monti di Creta, Rome, Italy

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Marco D’Agostino Istituto Dermopatico dell’Immacolata, IDI-IRCCS, Experimental Immunology Laboratory Via Monti di Creta, Rome, Italy

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Alessandra Carassiti Istituto Dermopatico dell’Immacolata, IDI-IRCCS, Experimental Immunology Laboratory Via Monti di Creta, Rome, Italy

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Guido Melillo Unit of Cardiology, IDI-IRCCS, Via Monti di Creta, Rome, Italy

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Alessandra Magenta Institute of Translational Pharmacology (IFT), National Research Council of Italy (CNR), Via Fosso del Cavaliere, Rome, Italy

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.e. IL17 and IL23) levels in psoriasis vulgaris patients and positively correlates with PASI ( 22 ). miR-200c was upregulated in endothelial cells (ECs) upon oxidative stress exposure and is responsible for apoptosis, senescence ( 23 ), nitric oxide (NO

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Stephen P Gray School of Cardiovascular Medicine & Sciences, King’s College London British Heart Foundation Centre, London, UK

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Ajay M Shah School of Cardiovascular Medicine & Sciences, King’s College London British Heart Foundation Centre, London, UK

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Ioannis Smyrnias School of Cardiovascular Medicine & Sciences, King’s College London British Heart Foundation Centre, London, UK

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senescence and apoptosis ( 43 ), an important step in the development of unstable lesions. It has also been demonstrated that in the setting of diabetes, NOX4 deletion results in a dedifferentiation of the SMC and increased proliferation ( 49 ). Additionally

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Laura Monteonofrio Laboratory of Cardiovascular Science, National Institute on Aging, National Institutes of Health, Baltimore, Maryland, USA

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Maria Cristina Florio Laboratory of Cardiovascular Science, National Institute on Aging, National Institutes of Health, Baltimore, Maryland, USA

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Majd AlGhatrif Laboratory of Cardiovascular Science, National Institute on Aging, National Institutes of Health, Baltimore, Maryland, USA
Longitudinal Study Section, National Institute on Aging, National Institutes of Health, Baltimore, Maryland, USA
Division of Cardiology, The Johns Hopkins University School of Medicine, Baltimore, Maryland, USA

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Edward G Lakatta Laboratory of Cardiovascular Science, National Institute on Aging, National Institutes of Health, Baltimore, Maryland, USA

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Maurizio C Capogrossi Laboratory of Cardiovascular Science, National Institute on Aging, National Institutes of Health, Baltimore, Maryland, USA
Division of Cardiology, The Johns Hopkins University School of Medicine, Baltimore, Maryland, USA

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TGF-β1. ROS are produced whereas NO bioavailability decreases with advancing age. Old VSMCs produce the AAASP, responsible for the underlying pro-inflammatory state, and exhibit enhanced proliferation, migration, senescence, and extracellular matrix

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