Telomere length and cardiovascular disease

Abstract

Telomeres are structures composed of deoxyribonucleic acid repeats that protect the end of chromosomes, but shorten with each cell division. They have been the subject of many studies, particularly in the field of oncology, and more recently their role in the onset, development and prognosis of cardiovascular disease has generated considerable interest. It has already been shown that these structures may deteriorate at the beginning of the atherosclerotic process, in the onset and development of arterial hypertension or during myocardial infarction, in which their length may be a predictor of outcome. As telomere length by its nature is a marker of cell senescence, it is of particular interest when studying the lifespan and fate of endothelial cells and cardiomyocytes, especially so because telomere length seems to be regulated by various factors notably certain cardiovascular risk factors, such as smoking, sex and obesity that are associated with high levels of oxidative stress. To gain insights into the links between telomere length and cardiovascular disease, and to assess the usefulness of telomere length as a new marker of cardiovascular risk, it seems essential to review the considerable amount of data published recently on the subject.

Is the Mean Blood Leukocyte Telomere Length a Predictor for Sporadic Thoracic Aortic Aneurysm? Data from a Preliminary Study

“…Shorter telomeres have been demonstrated in subjects with several CVD pathologies, including chronic heart failure, atherosclerosis, ventricular dysfunction, coronary artery calcification, and aortic valve stenosis. [6][7][8][9][10][11][12] Furthermore, telomere length has been also identified as an independent predictor of heart disease-related events. [6][7][8][9][10][11][12] In addition, a significant reduction in telomere content of AAA wall samples compared to normal aorta and in AAA patients than controls has been detected.…”

“…[6][7][8][9][10][11][12] Furthermore, telomere length has been also identified as an independent predictor of heart disease-related events. [6][7][8][9][10][11][12] In addition, a significant reduction in telomere content of AAA wall samples compared to normal aorta and in AAA patients than controls has been detected. 12,13 The mechanisms linking blood telomere attrition to CVD have been studied recently, 6 and number of potential explanations have been suggested.…”

“…[6][7][8][9][10][11] This assumption is based on the evidence that telomere content (the TTAGGG DNA repeats at the ends of chromosomes) in circulating blood leukocytes accurately reflects the biological age of the vascular wall, as recently demonstrated by Wilson et al 12 Furthermore, a series of recent epidemiological studies have demonstrated association of the reduction of blood telomere length with several CVD, such as AAA. [6][7][8][9][10][11][12] Patients with AAA showed a shorter leukocyte telomere length compared to controls, as verified by Atturu et al 13 In light of this evidence, our studies are aimed at determining whether the mean of blood leukocyte telomere length might be a predictor for S-TAA. 14 histopathological and phenotypic analyses, and exclusion criteria for syndromic and familial forms (e.g., Marfan and Ehler-Danlos syndromes) and autoimmune connective tissue disorders were used.…”

MiR-146a as marker of senescence-associated pro-inflammatory status in cells involved in vascular remodelling

“…Senescent endothelial cells are characterised by telomere shortening which occurs as a consequence of cellular replication and can be accelerated by harmful environmental factors, such as oxidative stress (Voghel et al 2007). When telomeres reach a critical threshold, endothelial cells become dysfunctional with an increased proinflammatory factors expression, resulting in a profile defined as 'senescence-associated secretory phenotype' (SASP) (Donato et al 2008;Sikora et al 2011;Saliques et al 2010). Secreted pro-inflammatory proteins acting in both autocrine and paracrine ways contribute to the senescent phenotype (Passos et al 2009).…”

Influence of endothelial dysfunction on telomere length in subjects with metabolic syndrome: LIPGENE study

“…They consist of several thousands of repetitive sequences of TTAGGG that are naturally shortened with each cell division due to the end replication problem (Nakashima et al 2004;Saliques et al 2010). Progressive attrition of telomeres leads to a critical length that triggers the cell arrest phenomenon known as senescence (Khan et al 2012), and due to the universal fact that telomere shorten with age, its study is crucial for understanding mechanisms of age-related diseases (Armanios 2013).…”