Chronic obstructive pulmonary disease (COPD) is a progressive disease characterized by destruction of lung tissue and airflow limitation, with smoking a key risk factor for development of the disease. COPD-induced declines in lung function have been associated with accelerated lung aging and cellular senescence. While it has been accepted that cell senescence generally is associated with shortening of telomeres, recent data has raised questions as to the validity of using telomere length as a biomarker of aging and/or telomere dysfunction. In the recent issue of AJP Lung, JodieBirch and colleagues at Newcastle University investigated the role of telomere dysfunction in the aging mouse lung and its potential role in cigarette smoke-induced COPD. In lung sections from COPD patients, the authors found that small airways epithelial cells contained more markers of senescence, including increased telomere-associated DNA damage foci (TAF) and reduced SIRT1 expression. Moreover, young mice exposed to cigarette smoke exhibited levels of TAF similar to that observed in the lungs of aged mice, and experiments performed in vitro confirmed that cigarette smoke extract increased TAF in small airways epithelial cells. Interestingly, telomere length was not significantly altered in these studies. While it is possible that small sample size masked an effect on telomere length, taken together, these results suggest that TAF are induced as a consequence of cigarette smoke exposure and may be a more robust signal of lung structural and functional decline in aging and with COPD.
To find out more about this interesting study, please check out the full text of this article. It is available for free on the AJP-Lung website, even for those with no subscription to APS journals:
Larrisa Shimoda- Associate Editor