Córdoba-Lanús Elizabeth, Cazorla-Rivero Sara, Espinoza-Jiménez Adriana, de-Torres Juan P, Pajares María J, Aguirre-Jaime Armando, Celli Bartolomé, Casanova Ciro
Research Unit, Hospital Universitario Nuestra Señora de Candelaria, Ctra. del Rosario 145, 38010, Santa Cruz de Tenerife, Spain.
Pulmonary Division, Clínica Universitaria de Navarra, Pamplona, Spain.
Respir Res. 2017 Apr 13;18(1):59. doi: 10.1186/s12931-017-0547-4.
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.
At baseline leukocyte telomere length was measured by qPCR in 121 smokers with COPD and 121 without COPD matched by age (T/S). The measurements were repeated in 70 of those patients with COPD and 73 non-COPD smokers after 3 years of follow up (T/S).
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/S = 0.66 ± 0.21 vs. T/S = 0.46 ± 0.16, p < 0.001, for the patients with COPD and T/S = 0.83 ± 0.56 vs. T/S = 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).
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.
慢性阻塞性肺疾病（COPD）可能与加速衰老有关。端粒缩短是衰老的生物标志物。横断面研究表明，与匹配的对照组相比，COPD患者的端粒更短。尚无研究描述端粒长度轨迹及其与COPD进展的关系。我们调查了COPD队列和无COPD的吸烟对照者端粒随时间的缩短情况及其与临床和肺功能参数的关系。
在基线时，通过qPCR测量了121例患有COPD的吸烟者和121例年龄匹配的无COPD吸烟者的白细胞端粒长度（T/S）。在随访3年后，对其中70例COPD患者和73例非COPD吸烟者重复进行测量（T/S）。
在初次测量时，与吸烟对照者相比，COPD患者的端粒更短（T/S = 0.68±0.25 vs. 0.88±0.52，p = 0.003），且与年龄和性别无关。在随访期间，我们观察到与吸烟对照者相比，COPD患者的端粒加速缩短（COPD患者的T/S = 0.66±0.21 vs. T/S = 0.46±0.16，p < 0.001，对照组的T/S = 0.83±0.56 vs. T/S = 0.74±0.52，p = 0.023；GLIM，p = 0.001）。这种缩短与基线端粒长度呈负相关（r = -0.49，p < 0.001）。在COPD患者中，未发现端粒长度变化率与肺功能变化之间存在显著关系（p > 0.05）。
与吸烟者相比，COPD患者的端粒缩短加速，且这种损耗率取决于基线端粒长度。此外，在3年的随访中，端粒长度及其缩短率与临床和肺功能参数变化无关。
