Publicaciones científicas

Telomere shortening and accelerated aging in COPD: findings from the BODE cohort

Elizabeth CL (1), Sara CR (2), Adriana EJ (2), de-Torres JP (3), María-José P (4), Armando AJ 2, Bartolomé C (5), Ciro C (2,6).
(1) Research Unit, Hospital Universitario Nuestra Señora de Candelaria, Ctra. del Rosario 145, 38010, Santa Cruz de Tenerife, Spain.
(2) Research Unit, Hospital Universitario Nuestra Señora de Candelaria, Ctra. del Rosario 145, 38010, Santa Cruz de Tenerife, Spain.
(3) Pulmonary Division, Clínica Universitaria de Navarra, Pamplona, Spain.
(4) Centro de Investigación Médica Aplicada (CIMA), UNAV, Pamplona, Spain.
(5) Pulmonary and Critical Care Department, Brigham and Women's Hospital, Boston, MA, USA.
(6) Pulmonary Division, Hospital Universitario Nuestra Señora de Candelaria, Santa Cruz de Tenerife, Spain. 

Revista: Respiratory Research

Fecha: 13/04/2017

Neumología

BACKGROUND:
Chronic 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.

METHODS:
At 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).

RESULTS:
At 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).

CONCLUSIONS:
Compared 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.

CITA DEL ARTÍCULO  Respir Res. 2017 Apr 13;18(1):59. doi: 10.1186/s12931-017-0547-4

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