Rate of telomere shortening and cardiovascular damage: a longitudinal study in the 1946 British Birth Cohort.
Rate of telomere shortening and cardiovascular damage: a longitudinal study in the 1946 British Birth Cohort.
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端粒缩短和心血管损伤的速度：1946年英国出生队列的纵向研究。
DOI：
10.1093/eurheartj/ehu226
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发表时间：
2014-12-07
影响因子：
39.3
通讯作者：
NSHD scientific and data collection teams
中科院分区：
文献类型：
--
作者：
Masi S;D'Aiuto F;Martin-Ruiz C;Kahn T;Wong A;Ghosh AK;Whincup P;Kuh D;Hughes A;von Zglinicki T;Hardy R;Deanfield JE;NSHD scientific and data collection teams
横断面研究报告了较短的白细胞端粒长度(LTL)与血管和心脏损伤的测量之间的关系。然而，LTL动力学在与年龄相关的心血管重构过程中的作用仍不清楚。在这项研究中，我们探讨了LTL缩短率是否可以预测10年后的心血管表型，以及已建立的心血管危险因素对这种关系的影响。所有参加MRC全国健康与发展调查的参与者包括53岁和60岁的年龄段的LTL和传统的心血管危险因素，以及60岁的年龄段的颈总动脉内中膜厚度、心脏重量和左心功能。通过实时聚合酶链式反应测量LTL，并在两个时间点在1033名个体中获得。53岁的LTL与60-岁的CV型无关，而与60-岁的CIMT呈负相关(β=−0.017，P=0.015)。然而，53岁至60岁年龄段的端粒缩短率与60岁年龄段的CIMT值之间的相关性最强(β=−0.020，P=0.006)。这种关联性不受传统心血管风险因素调整的影响。心脏测量与LTL的横断面或纵向测量无关。这些发现表明，中年后期细胞老化的进展速度(由LTL磨损率反映)与血管损伤有关，独立于心血管风险因素暴露的贡献。
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. 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. 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.
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影响因子：
64.5
作者：
López-Otín C;Blasco MA;Partridge L;Serrano M;Kroemer G
通讯作者：
Kroemer G
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作者：
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Briet, Marie
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作者：
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通讯作者：
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