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Rate of Telomere Shortening and Cardiovascular Damage: A Longitudinal Study in the 1946 British Birth Cohort
Study Questions:
What is relationship between leukocyte telomere length (LTL) shortening and cardiovascular (CV) phenotypes?
Methods:
Participants from a 1946 British Birth Cohort with measures of LTL, CV risk factors at ages 53 and 60-64 years, and carotid intima-media thickness (cIMT), cardiac mass, and left ventricular (LV) function at ages 60-64 years were included. LTL was measured by real-time polymerase chain reaction and available at both time points in 1,033 individuals.
Results:
LTL at age 53 years was not linked with any CV phenotype at age 60-64 years, although a negative association was found between LTL and cIMT at age 60–64 years (β = –0.017; p = 0.015). The strongest association was found between rate of telomere shortening between ages 53 and 60-64 years and values of cIMT at ages 60-64 years (β = –0.020, p = 0.006). This association was not affected by CV risk factor adjustment. Cardiac measurements were not associated with cross-sectional or longitudinal measures of LTL.
Conclusions:
The authors concluded that rate of progression of cellular aging in late midlife relates to vascular damage, independently from contribution of CV risk factor exposure.
Perspective:
Telomeres are repetitive nucleotide sequences that cap chromosomes, protecting them from deterioration and fusion. Telomeres progressively shorten with cellular replication and this shortening is associated with age-related diseases, although causal relationships between telomere shortening and disease remain unclear. This long-term study demonstrates a small, but significant association of leukocyte telomere shortening with cIMT but not LV mass, raising the possibility that there are independent effects of cellular aging on pathways involved in vascular disease.
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