Inflammation and Vascular Ageing: From Telomeres to Novel Emerging Mechanisms
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REVIEW ARTICLE
Inflammation and Vascular Ageing: From Telomeres to Novel Emerging Mechanisms Martina Chiriacò1 · Georgios Georgiopoulos2 · Emiliano Duranti1 · Luca Antonioli1 · Ilaria Puxeddu1 · Monica Nannipieri1 · Javier Rosada3 · Corrado Blandizzi1 · Stefano Taddei1 · Agostino Virdis1 · Stefano Masi1,4,5 Received: 19 March 2019 / Accepted: 12 July 2019 © Italian Society of Hypertension 2019
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. Keywords Cardiovascular continuum · Ageing · Inflammation · Telomeres · CHIP
1 Introduction Acute inflammatory responses evoked by tissue and cellular damage exert beneficial effects as they promote tissue repair and help to prevent colonization of the damaged tissues by opportunistic pathogens. Thus, a limited temporal evolution This article is part of the topical collection on Vascular Aging and Arterial Stiffness. * Stefano Masi [email protected] 1
Department of Clinical and Experimental Medicine, Università di Pisa, Santa Chiara Hospital, Via Roma, 67, 56126 Pisa, Italy
2
First Department of Cardiology, Hippokration Hospital, University of Athens, Athens, Greece
3
Fourth Unit of Internal Medicine, University Hospital of Pisa, Pisa, Italy
4
The National Centre for Cardiovascular Preventions and Outcomes, Institute of Cardiovascular Science, University College London, London, UK
5
Department of Twin Research and Genetic Epidemiology, King’s College London, London, UK
of the inflammatory processes is considered beneficial as it enables the elimination of the triggering insult and promotes tissue repair. Conversely, persistent inflammatory stimuli or dysregulation of mechanisms involved in the resolution of acute inflammatory responses result in a chronic inflammatory exposure, which is commonly observed in ageing and several age-related disea
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