Rate of telomere shortening and cardiovascular damage: A longitudinal study in the 1946 British Birth Cohort
| Autor: | Masi, Stefano, D'Aiuto, Francesco, Martin-Ruiz, Carmen, Kahn, Tauseef, Wong, Andrew, Ghosh, Arjun K., Whincup, Peter, Kuh, Diana, Hughes, Alan, von Zglinicki, Thomas, Hardy, Rebecca, Deanfield, John Eric |
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| Jazyk: | angličtina |
| Rok vydání: | 2014 |
| Předmět: |
Carotid Artery Diseases
Male Cardiac & Cardiovascular Systems Prevention and Epidemiology BIOLOGY INTIMA-MEDIA THICKNESS 1102 Cardiovascular Medicine And Haematology Carotid Intima-Media Thickness Clinical Research Risk Factors LENGTH Leukocytes Humans Longitudinal Studies Telomeres shortening Cellular Senescence Telomere Shortening AMERICAN-SOCIETY RISK Science & Technology VASCULAR-DISEASE OLDEST-OLD ASSOCIATION Middle Aged Ageing Cardiovascular diseases Phenotype ATHEROSCLEROSIS Cardiovascular System & Hematology NSHD scientific and data collection teams Cell Aging Cardiovascular System & Cardiology Disease Progression HEART Carotid artery Cardiovascular Diseases Female Cardiology and Cardiovascular Medicine Life Sciences & Biomedicine |
| Zdroj: | European Heart Journal |
| Popis: | Aim Cross-sectional studies reported associations between short leucocyte telomere length (LTL) and measures of vascular and cardiac damage. However, the contribution of LTL dynamics to the age-related process of cardiovascular (CV) remodelling remains unknown. In this study, we explored whether the rate of LTL shortening can predict CV phenotypes over 10-year follow-up and the influence of established CV risk factors on this relationship. Methods and results All the participants from the MRC National Survey of Health and Development (NSHD) with measures of LTL and traditional CV risk factors at 53 and 60–64 years and common carotid intima-media thickness (cIMT), cardiac mass and left ventricular function at 60–64 years were included. LTL was measured by real-time polymerase chain reaction and available at both time points in 1033 individuals. While LTL at 53 years was not linked with any CV phenotype at 60–64 years, a negative association was found between LTL and cIMT at 60–64 years (β = −0.017, P = 0.015). However, the strongest association was found between rate of telomere shortening between 53 and 60–64 years and values of cIMT at 60–64 years (β = −0.020, P = 0.006). This association was not affected by adjustment for traditional CV risk factors. Cardiac measurements were not associated with cross-sectional or longitudinal measures of LTL. Conclusion These findings suggest that the rate of progression of cellular ageing in late midlife (reflected by the rate of LTL attrition) relates to vascular damage, independently from contribution of CV risk factor exposure. |
| Databáze: | OpenAIRE |
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