The relationship between telomere length and putative markers of vascular ageing: A systematic review and meta-analysis

Kosmopoulos, Marinos; Chiriacò, Martina; Stamatelopoulos, Kimon; Tsioufis, Costas; Masci, Pier Giorgio; Kontogiannis, Christos; Mengozzi, Alessandro; Pugliese, Nicola Riccardo; Taddei, Stefano; Virdis, Agostino; Masi, Stefano; Georgiopoulos, Georgios

doi:10.1016/j.mad.2021.111604

Cited by 11 publications

(10 citation statements)

References 84 publications

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“…52 Elevated plasma IL-6 concentrations are a hallmark of persistent low-level ‘sterile’ inflammation related to unhealthy ageing, which is characterized by an augmented risk of metabolic and CVD (‘inflamm-ageing’). 180 , 181 Indeed, IL-6 can increase vascular smooth muscle cell stiffness and mitochondrial dysfunction, which explains the link between inflammation and impaired vascular function. 52 , 182 Interestingly, Tet-2-mutated macrophages secrete higher amounts of IL-6, and these mutations are frequently seen in clonal haematopoiesis of indeterminate potential (CHIP), which is associated with an increased risk of cardiovascular events.…”

Section: Emerging Anti-inflammatory Targets With Potential Benefit In...mentioning

confidence: 99%

Inflammatory pathways in heart failure with preserved left ventricular ejection fraction: implications for future interventions

Pugliese

Pellicori

Filidei

et al. 2022

Cardiovascular Research

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Many patients with symptoms and signs of heart failure have a left ventricular ejection fraction ≥50%, termed heart failure with preserved ejection fraction (HFpEF). HFpEF is a heterogeneous syndrome mainly affecting older people who have many other cardiac and non-cardiac conditions that often cast doubt on the origin of symptoms, such as breathlessness, or signs, such as peripheral oedema, rendering them neither sensitive nor specific to the diagnosis of HFpEF. Currently, management of HFpEF is mainly directed at controlling symptoms and treating comorbid conditions such as hypertension, atrial fibrillation, anaemia and coronary artery disease. HFpEF is also characterised by a persistent increase in inflammatory biomarkers. Inflammation may be a key driver of the development and progression of HFpEF and many of its associated comorbidities. Detailed characterisation of specific inflammatory pathways may provide insights into the pathophysiology of HFpEF and guide its future management. There is growing interest in novel therapies specifically designed to target deregulated inflammation in many therapeutic areas, including cardiovascular disease. However, large-scale clinical trials investigating the effectiveness of anti-inflammatory treatments in HFpEF are still lacking. In this manuscript, we review the role of inflammation in HFpEF and the possible implications for future trials.

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Section: Emerging Anti-inflammatory Targets With Potential Benefit In...mentioning

confidence: 99%

Inflammatory pathways in heart failure with preserved left ventricular ejection fraction: implications for future interventions

Pugliese

Pellicori

Filidei

et al. 2022

Cardiovascular Research

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“…That individuals age at different rates is not currently captured by traditional regression-based risk equations as they assume all individuals in the population age at the same rate. The traditional equations are therefore insensitive to the variation in individual risk that results from biological aging, and it has therefore been suggested that biological markers such as Leukocyte telomere length (LTL) and DNA methylation rates could be used to refine the prediction of an individual's ASCVD risk [11][12][13][14] .…”

Section: Introductionmentioning

confidence: 99%

WITHDRAWN: Comparison of Leucocyte Telomere Length, Atherosclerotic Cardiovascular disease risk and the output of a Deep learning Cardiac BioAge risk prediction tool: A UK Biobank Cohort study

Vaghefi,

An,

Corbett

et al. 2024

Preprint

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Significance. That a retinal image based Deep Learning (DL) Cardiac BioAge Model may be a useful novel tool that can personalise an individuals risk of Atherosclerotic cardiovascular disease (ASCVD) events. Purpose. To determine whether the results issued by our DL Cardiac BioAge model are consistent with the known trends of cardiovascular disease (CVD) risk and the biomarker Leucocyte Telomere Length, in a cohort of individuals from the UK Biobank. Methods. Individuals were divided by sex, ranked by Z adjusted log T/S Leucocyte Telomere length (LTL) and then grouped into deciles. The retinal images were then presented to the DL model and individuals Cardiac BioAges determined. Individuals within each LTL decile was then ranked by Cardiac BioAge, and the mean of the CVD risk biomarkers in the top and bottom quartiles compared. The relationship between an individuals Cardiac BioAge, the CVD biomarkers and LTL were determined using traditional correlation statistics. Results. The DL Cardiac BioAge model was able to accurately stratify individuals by the traditional CVD risk biomarkers, and for both males and females those issued with a Cardiac BioAge in the top quartile of their chronological peer group had a significantly higher mean SBP, HbA1C and 10-year Pooled Cohort Equation ASCVD scores compared to those individuals in the bottom quartile. Cardiac BioAge was associated with LTL shortening for both males and females. (Males: -0.220, P <0.001; Females: -0.174, P <0.001) Conclusion In this small cohort study increasing CVD risk; as assessed by both traditional biomarkers, ASCVD risk scoring and a DL Cardiac BioAge CVD risk model, was inversely related to LTL. At a population level our data supports the growing body of evidence that suggests that LTL shortening is a surrogate marker for increasing CVD risk and that this risk can be captured by our novel DL Cardiac BioAge model.

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“…These findings support the notion that telomere shortening could potentially cause microvascular dysfunction, which is an early feature of atherosclerosis and vascular diseases [ 70 ]. Although experimental studies have suggested that telomere function is a crucial determinant of microvascular function [ 44 , 49 , 71 – 74 ], and some studies have shown that telomere length is related to other subclinical markers of atherosclerosis [ 35 , 75 , 76 ], only a few clinical and epidemiological studies have investigated the association of telomere length with microvascular function [ 28 , 29 ]. One cross-sectional study in 102 patients with a history of cerebrovascular diseases found shortened telomeric 3’-overhang (G-tail), but not telomere length, to be associated with microvascular function [ 29 ].…”

Section: Discussionmentioning

confidence: 99%

Associations of measured and genetically predicted leukocyte telomere length with vascular phenotypes: a population-based study

Liu,

Aziz,

Imtiaz

et al. 2023

GeroScience

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Shorter leukocyte telomere length (LTL) is associated with cardiovascular dysfunction. Whether this association differs between measured and genetically predicted LTL is still unclear. Moreover, the molecular processes underlying the association remain largely unknown. We used baseline data of the Rhineland Study, an ongoing population-based cohort study in Bonn, Germany [56.2% women, age: 55.5 ± 14.0 years (range 30 – 95 years)]. We calculated genetically predicted LTL in 4180 participants and measured LTL in a subset of 1828 participants with qPCR. Using multivariable regression, we examined the association of measured and genetically predicted LTL, and the difference between measured and genetically predicted LTL (ΔLTL), with four vascular functional domains and the overall vascular health. Moreover, we performed epigenome-wide association studies of three LTL measures. Longer measured LTL was associated with better microvascular and cardiac function. Longer predicted LTL was associated with better cardiac function. Larger ΔLTL was associated with better microvascular and cardiac function and overall vascular health, independent of genetically predicted LTL. Several CpGs were associated (p < 1e-05) with measured LTL (n = 5), genetically predicted LTL (n = 8), and ΔLTL (n = 27). Genes whose methylation status was associated with ΔLTL were enriched in vascular endothelial signaling pathways and have been linked to environmental exposures, cardiovascular diseases, and mortality. Our findings suggest that non-genetic causes of LTL contribute to microvascular and cardiac function and overall vascular health, through an effect on the vascular endothelial signaling pathway. Interventions that counteract LTL may thus improve vascular function.

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The relationship between telomere length and putative markers of vascular ageing: A systematic review and meta-analysis

Cited by 11 publications

References 84 publications

Inflammatory pathways in heart failure with preserved left ventricular ejection fraction: implications for future interventions

Inflammatory pathways in heart failure with preserved left ventricular ejection fraction: implications for future interventions

WITHDRAWN: Comparison of Leucocyte Telomere Length, Atherosclerotic Cardiovascular disease risk and the output of a Deep learning Cardiac BioAge risk prediction tool: A UK Biobank Cohort study

Associations of measured and genetically predicted leukocyte telomere length with vascular phenotypes: a population-based study

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