Abstract
BackgroundChronic Obstructive Pulmonary Disease (COPD) may be associated with accelerated aging. Telomere shortening is a biomarker of aging. Cross-sectional studies describe shorter telomeres in COPD compared with matched controls. No studies have described telomere length trajectory and its relationship with COPD progression. We investigated telomere shortening over time and its relationship to clinical and lung function parameters in a COPD cohort and smoker controls without COPD.MethodsAt baseline leukocyte telomere length was measured by qPCR in 121 smokers with COPD and 121 without COPD matched by age (T/S0). The measurements were repeated in 70 of those patients with COPD and 73 non-COPD smokers after 3 years of follow up (T/S3).ResultsAt initial measurement, telomeres were shorter in COPD patients when compared to smoker controls (T/S = 0.68 ± 0.25 vs. 0.88 ± 0.52, p = 0.003) independent from age and sex. During the follow-up period, we observed an accelerated telomere shortening in individuals with COPD in contrast to smoker controls (T/S0 = 0.66 ± 0.21 vs. T/S3 = 0.46 ± 0.16, p < 0.001, for the patients with COPD and T/S0 = 0.83 ± 0.56 vs. T/S3 = 0.74 ± 0.52, p = 0.023 for controls; GLIM, p = 0.001). This shortening was inversely related to the baseline telomere length (r = −0.49, p < 0.001). No significant relationship was found between the rate of change in telomere length and change in lung function in the patients with COPD (p > 0.05).ConclusionsCompared with smokers, patients with COPD have accelerated telomere shortening and this rate of attrition depends on baseline telomere length. Furthermore, the telomere length and its rate of shortening did not relate to clinical and lung function parameters changes over 3 years of follow-up.
Highlights
Chronic Obstructive Pulmonary Disease (COPD) may be associated with accelerated aging
Telomere length measured by the the reference single copy gene (T/S) ratio inversely correlated with age in COPD (r = −0.21; p = 0.02) and in smoker controls (r = −0.19; p = 0.02)
This longitudinal study shows that COPD patients experience an accelerated telomere shortening process compared with smokers without COPD and this telomere attrition occurs in close relation to baseline telomere length
Summary
Chronic Obstructive Pulmonary Disease (COPD) may be associated with accelerated aging. Telomere shortening is a biomarker of aging. No studies have described telomere length trajectory and its relationship with COPD progression. We investigated telomere shortening over time and its relationship to clinical and lung function parameters in a COPD cohort and smoker controls without COPD. It has been suggested that COPD is a disease of accelerated aging [4, 5] and telomere length has been proposed as a biomarker of aging [6, 7]. Because the DNA cannot be duplicated at the end of the chromosome, each duplication results in its shortening. Telomeres get progressively shorter as cells divide, an event that is known as the end-replication process. Other mechanisms may account for the accelerated loss of telomeres, such as the DNA damage induced by oxidative stress [8]
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