Por favor, use este identificador para citar o enlazar este Item:http://hdl.handle.net/20.500.12105/16410
Título
Subclinical atherosclerosis and accelerated epigenetic age mediated by inflammation: a multi-omics study.
Autor(es)
Sanchez-Cabo, Fatima CNIC | Fuster, Valentin CNIC | Silla-Castro, Juan Carlos CNIC | González, Gema | Lorenzo-Vivas, Erika | Álvarez, Rebeca | Callejas, Sergio CNIC | Benguria, Alberto CNIC | Gil, Eduardo | Nunez, Estefania CNIC | Oliva, Belen CNIC | Mendiguren, José María | Cortes-Canteli, Marta CNIC | Bueno, Hector CNIC | Andres, Vicente CNIC | Ordovás, Jose María | Fernandez-Friera, Leticia CNIC | Quesada, Antonio J | Garcia, Jose Manuel | Rossello, Xavier CNIC | Vazquez, Jesus CNIC | Dopazo, Ana CNIC | Fernández-Ortiz, Antonio | Ibáñez, Borja CNIC | Fuster, Jose Javier | Lara-Pezzi, Enrique CNIC
Fecha de publicación
2023-08-01
Cita
Eur Heart J. 2023 Aug 1;44(29):2698-2709.
Idioma
Inglés
Tipo de documento
journal article
Resumen
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.
MESH
Atherosclerosis | Coronary Artery Disease | Middle Aged | Humans | Multiomics | Inflammation | Epigenesis, Genetic | Risk Factors
Versión en línea
DOI
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