Atherosclerosis is a disease of ageing in that its incidence and prevalence increase with age. However, atherosclerosis is also associated with biological ageing, manifest by a number of typical hallmarks of ageing in the atherosclerotic plaque. Thus, accelerated biological ageing may be superimposed on the effects of chronological ageing in atherosclerosis. Tissue ageing is seen in all cells that comprise the plaque, but particularly in vascular smooth muscle cells (VSMCs). Hallmarks of ageing include evidence of cell senescence, DNA damage (including telomere attrition), mitochondrial dysfunction, a pro-inflammatory secretory phenotype, defects in proteostasis, epigenetic changes, deregulated nutrient sensing, and exhaustion of progenitor cells. In this model, initial damage to DNA (genomic, telomeric, mitochondrial and epigenetic changes) results in a number of cellular responses (cellular senescence, deregulated nutrient sensing and defects in proteostasis). Ultimately, ongoing damage and attempts at repair by continued proliferation overwhelm reparative capacity, causing loss of specialised cell functions, cell death and inflammation. This review summarises the evidence for accelerated biological ageing in atherosclerosis,...Continue Reading
Reduction of nitric oxide producing activity associated with in vitro aging in cultured human umbilical vein endothelial cell
Apoptosis of human vascular smooth muscle cells derived from normal vessels and coronary atherosclerotic plaques
Proliferation in primary and restenotic coronary atherectomy tissue. Implications for antiproliferative therapy
Cooperative interactions between RB and p53 regulate cell proliferation, cell senescence, and apoptosis in human vascular smooth muscle cells from atherosclerotic plaques
Oxidative DNA damage and repair in experimental atherosclerosis are reversed by dietary lipid lowering
Defect in insulin-like growth factor-1 survival mechanism in atherosclerotic plaque-derived vascular smooth muscle cells is mediated by reduced surface binding and signaling
Differential cyclin E expression in human in-stent stenosis smooth muscle cells identifies targets for selective anti-restenosis therapy
Abundant progenitor cells in the adventitia contribute to atherosclerosis of vein grafts in ApoE-deficient mice
DNA methylation polymorphisms precede any histological sign of atherosclerosis in mice lacking apolipoprotein E.
Statins enhance migratory capacity by upregulation of the telomere repeat-binding factor TRF2 in endothelial progenitor cells
Detection of mtDNA with 4977 bp deletion in blood cells and atherosclerotic lesions of patients with coronary artery disease
Epigenetic basis for the transcriptional hyporesponsiveness of the human inducible nitric oxide synthase gene in vascular endothelial cells
Vascular smooth muscle cells undergo telomere-based senescence in human atherosclerosis: effects of telomerase and oxidative stress
Pot1 deficiency initiates DNA damage checkpoint activation and aberrant homologous recombination at telomeres
Smooth muscle cells in atherosclerosis originate from the local vessel wall and not circulating progenitor cells in ApoE knockout mice
Telomere length, risk of coronary heart disease, and statin treatment in the West of Scotland Primary Prevention Study: a nested case-control study
Effects of aging and hypoxia-inducible factor-1 activity on angiogenic cell mobilization and recovery of perfusion after limb ischemia
Angiotensin II-mediated oxidative DNA damage accelerates cellular senescence in cultured human vascular smooth muscle cells via telomere-dependent and independent pathways.
Age decreases endothelial progenitor cell recruitment through decreases in hypoxia-inducible factor 1alpha stabilization during ischemia
Statins use a novel Nijmegen breakage syndrome-1-dependent pathway to accelerate DNA repair in vascular smooth muscle cells
Premature senescence of highly proliferative endothelial progenitor cells is induced by tumor necrosis factor-alpha via the p38 mitogen-activated protein kinase pathway.
Absence of Akt1 reduces vascular smooth muscle cell migration and survival and induces features of plaque vulnerability and cardiac dysfunction during atherosclerosis.
Circulating endothelial progenitor cells do not contribute to plaque endothelium in murine atherosclerosis
Accumulation of Smooth Muscle 22α Protein Accelerates Senescence of Vascular Smooth Muscle Cells via Stabilization of p53 In Vitro and In Vivo
Temporal trends, characteristics and outcomes of fibrinolytic therapy for ST-elevation myocardial infarction among patients 80 years or older
Microvascular contributions to age-related macular degeneration (AMD): from mechanisms of choriocapillaris aging to novel interventions
Foam cell origination from degenerated vascular smooth muscle cells in atherosclerosis: An ultrastructural study on hyperlipidemic rabbits
Prednisolone suppresses adriamycin-induced vascular smooth muscle cell senescence and inflammatory response via the SIRT1-AMPK signaling pathway
Quercetin Attenuates Atherosclerosis via Modulating Oxidized LDL-Induced Endothelial Cellular Senescence
Inflammatory Drivers of Cardiovascular Disease: Molecular Characterization of Senescent Coronary Vascular Smooth Muscle Cells
Involvement of Flavonoids from the Leaves of Carya cathayensis Sarg. in Sirtuin 1 Expression in HUVEC Senescence
Hypertension and Age-Related Cognitive Impairment: Common Risk Factors and a Role for Precision Aging
Nitric oxide-heat shock protein axis in menopausal hot flushes: neglected metabolic issues of chronic inflammatory diseases associated with deranged heat shock response
Endothelial sprouting, proliferation, or senescence: tipping the balance from physiology to pathology.
Sirtuin 6 deficiency induces endothelial cell senescence via downregulation of forkhead box M1 expression.
Comparison of the ATRIA, CHA2DS2-VASc, and Modified Scores ATRIA-HSV, CHA2DS2-VASc-HS, for the Prediction of Coronary Artery Disease Severity.
Bupleurum chinense Polysaccharide Improves LPS-Induced Senescence of RAW264.7 Cells by Regulating the NF-κ B Signaling Pathway
The effect of chronic intermittent hypoxia in cardiovascular gene expression is modulated by age in a mice model of sleep apnea.
Telomere damage promotes vascular smooth muscle cell senescence and immune cell recruitment after vessel injury.
Anagliptin prevented interleukin 1β (IL-1β)-induced cellular senescence in vascular smooth muscle cells through increasing the expression of sirtuin1 (SIRT1).
Regular, Intense Exercise Training as a Healthy Aging Lifestyle Strategy: Preventing DNA Damage, Telomere Shortening and Adverse DNA Methylation Changes Over a Lifetime.
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