TY - JOUR
TI - Inflammation and Vascular Ageing: From Telomeres to Novel Emerging Mechanisms
AU - Chiriacò, M.
AU - Georgiopoulos, G.
AU - Duranti, E.
AU - Antonioli, L.
AU - Puxeddu, I.
AU - Nannipieri, M.
AU - Rosada, J.
AU - Blandizzi, C.
AU - Taddei, S.
AU - Virdis, A.
AU - Masi, S.
JO - High Blood Pressure and Cardiovascular Prevention
PY - 2019
VL - 26
TODO - 4
SP - 321-329
PB - Springer International Publishing
SN - 1120-9879, 1179-1985
TODO - 10.1007/s40292-019-00331-7
TODO - aging;  atherosclerosis;  cardiovascular disease;  chronic inflammation;  disease association;  hematopoiesis;  human;  inflammation;  inflammatory disease;  leukocyte;  nonhuman;  pathogenesis;  priority journal;  Review;  telomere;  telomere length;  age;  aging;  animal;  cardiovascular disease;  cell aging;  genetics;  inflammation;  metabolism;  pathology;  pathophysiology;  risk assessment;  risk factor;  signal transduction;  telomere;  telomere homeostasis;  telomere shortening;  time factor, autacoid, Age Factors;  Aging;  Animals;  Cardiovascular Diseases;  Cellular Senescence;  Humans;  Inflammation;  Inflammation Mediators;  Risk Assessment;  Risk Factors;  Signal Transduction;  Telomere;  Telomere Homeostasis;  Telomere Shortening;  Time Factors
TODO - Cardiovascular disease (CVD) remains the leading cause of morbility and mortality worldwide. The identification of common cardiovascular risk factors has led to the development of effective treatments that enabled a significant reduction of the global cardiovascular disease burden. However, a significant proportion of cardiovascular risk remains unexplained by these risk factors leaving many individuals at risk of cardiovascular events despite good control of the risk factors. Recent randomized clinical trials and Mendelian randomization studies have suggested that inflammation explains a significant proportion of the residual cardiovascular risk in subjects with good control of risk factors. An accelerated process of vascular ageing is increasingly recognized as a potential mechanism by which inflammation might increase the risk of CVD. In turn, cellular ageing represents an important source of inflammation within the vascular wall, potentially creating a vicious cycle that might promote progression of atherosclerosis, independently from the individual cardiovascular risk factor burden. In this review, we summarise current evidence suggesting a role for biological ageing in CVD and how inflammation might act as a key mediator of this association. © 2019, Italian Society of Hypertension.
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