['Fibroblast growth factor\u200923 knockout mice develop premature aging and emphysema, indicating that dysregulation of the normal aging process is involved in the pathobiology of chronic obstructive pulmonary disease. Thus, we explored the association among a coding single-nucleotide polymorphism of fibroblast growth factor\u200923, its protein concentration in serum and telomere length in patients with chronic obstructive pulmonary disease.', 'The study involved 361 smokers; among whom, 244 were patients with chronic obstructive pulmonary disease. We genotyped a coding single-nucleotide polymorphism of fibroblast growth factor\u200923, rs7955866, and measured the telomere length of the peripheral blood cells. We also determined emphysema severity and airflow obstruction using computed tomography and pulmonary function tests, respectively. Furthermore, we analyzed the association between the disease phenotypes and fibroblast growth factor\u200923 genotypes or telomere length of peripheral blood leukocytes, as well as the association between the serum level of the studied protein and its genotypes.', 'The mice with A\u2009alleles on rs7955866 showed severe upper lung emphysema (P\u2009=\u20090.008). The serum concentration of the tested protein was lower in the mice with A\u2009allele than in the G\u2009homozygotes (P\u2009=\u20090.004). Telomere shortening was associated with airflow obstruction (P\u2009=\u20090.009), but not with upper lung emphysema.'] Is senescence involved in the pathogenesis of chronic obstructive pulmonary disease through effects on telomeres and the anti-aging molecule fibroblast growth factor 23?