| Literature DB >> 31325087 |
Martina Chiriacò1, Georgios Georgiopoulos2, Emiliano Duranti1, Luca Antonioli1, Ilaria Puxeddu1, Monica Nannipieri1, Javier Rosada3, Corrado Blandizzi1, Stefano Taddei1, Agostino Virdis1, Stefano Masi4,5,6.
Abstract
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.Entities:
Keywords: Ageing; CHIP; Cardiovascular continuum; Inflammation; Telomeres
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Year: 2019 PMID: 31325087 DOI: 10.1007/s40292-019-00331-7
Source DB: PubMed Journal: High Blood Press Cardiovasc Prev ISSN: 1120-9879