Rate of Telomere Shortening and Cardiovascular Damage: A Longitudinal Study in the 1946 British Birth Cohort
What is relationship between leukocyte telomere length (LTL) shortening and cardiovascular (CV) phenotypes?
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.
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.
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.
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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