"We found that cells with damaged DNA stopped dividing, and lung cells with too much damage could no longer be repaired, thus contributing to the emphysema," she continued. "These results are one of the clearest examples of telomere length, which is an inherited factor, interacting with an environmental insult to cause disease. In fact, our results in mice suggest that short telomeres might contribute to how cigarette smoke accelerates aging in the lung in some individuals."
Dr. Armanios hopes that this new research will lead into new insights into identifying new ways to preserve lung function with age.
"It's important to remember that there is no good reason to smoke and the best way to prevent emphysema is to stop smoking," she said.
Previously, Dr. Armanios and her group had shown that shortened telomeres cause a disease known as idiopathic pulmonary fibrosis (IPF), a disorder of unrelenting scarring in the lung. IPF occurs with emphysema in some individuals, and the incidence of both disorders increases with age and with smoking. "By linking telomere length to both disorders, there is now clear suggestion that they may share a common mechanism that can be traced to telomeres."
Further research must be done to confirm that the observed findings are applicable to humans, and, if so, what mechanisms might underlie them. "Now that we have examined the question of susceptibility in a rigorous genetic model, we can begin to study how telomere length affects emphysema risk in susceptible populations."
|Contact: Keely Savoie|
American Thoracic Society