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Ornella Colpani and Gaia Spinetti

). 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

Open access

Ka Ka Ting, Paul Coleman, Yang Zhao, Mathew A Vadas, and Jennifer R Gamble

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

Open access

Amer Harky, Ka Siu Fan, and Ka Hay Fan

-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

Open access

Alessandra Magenta, Reggio Lorde, Sunayana Begum Syed, Maurizio C Capogrossi, Annibale Puca, and Paolo Madeddu

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

Open access

Sarah Costantino, Shafeeq A Mohammed, Samuele Ambrosini, and Francesco Paneni

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.

Open access

Stephen P Gray, Ajay M Shah, and Ioannis Smyrnias

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

Open access

Laura Monteonofrio, Maria Cristina Florio, Majd AlGhatrif, Edward G Lakatta, and Maurizio C Capogrossi

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