Subclinical atherosclerosis and accelerated epigenetic age mediated by inflammation: a multi-omics study

表观遗传学 医学 亚临床感染 炎症 生物信息学 疾病 内科学 遗传学 生物 基因
作者
Fátima Sánchez‐Cabo,Valentı́n Fuster,Juan Carlos Silla-Castro,Gema González,Erika Lorenzo-Vivas,Rebeca Álvarez,Sergio Callejas,Alberto Benguría,Eduardo Gil,Estefanía Núñez,Belén Oliva,José M. Mendiguren,Marta Cortés‐Canteli,Héctor Bueno,Vicente Andrés,José M. Ordovás,Leticia Fernández‐Friera,Antonio J. Quesada,José M. Garcia,Xavier Rosselló,Jesús Vázquez,Ana Dopazo,Antonio Fernández-Ortı́z,Borja Ibáñez,José J. Fuster,Enrique Lara‐Pezzi
出处
期刊:European Heart Journal [Oxford University Press]
卷期号:44 (29): 2698-2709 被引量:43
标识
DOI:10.1093/eurheartj/ehad361
摘要

Abstract Aims Epigenetic age is emerging as a personalized and accurate predictor of biological age. The aim of this article is to assess the association of subclinical atherosclerosis with accelerated epigenetic age and to investigate the underlying mechanisms mediating this association. Methods and results Whole blood methylomics, transcriptomics, and plasma proteomics were obtained for 391 participants of the Progression of Early Subclinical Atherosclerosis study. Epigenetic age was calculated from methylomics data for each participant. Its divergence from chronological age is termed epigenetic age acceleration. Subclinical atherosclerosis burden was estimated by multi-territory 2D/3D vascular ultrasound and by coronary artery calcification. In healthy individuals, the presence, extension, and progression of subclinical atherosclerosis were associated with a significant acceleration of the Grim epigenetic age, a predictor of health and lifespan, regardless of traditional cardiovascular risk factors. Individuals with an accelerated Grim epigenetic age were characterized by an increased systemic inflammation and associated with a score of low-grade, chronic inflammation. Mediation analysis using transcriptomics and proteomics data revealed key pro-inflammatory pathways (IL6, Inflammasome, and IL10) and genes (IL1B, OSM, TLR5, and CD14) mediating the association between subclinical atherosclerosis and epigenetic age acceleration. Conclusion The presence, extension, and progression of subclinical atherosclerosis in middle-aged asymptomatic individuals are associated with an acceleration in the Grim epigenetic age. Mediation analysis using transcriptomics and proteomics data suggests a key role of systemic inflammation in this association, reinforcing the relevance of interventions on inflammation to prevent cardiovascular disease.
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