Animal studies have shown that shortened telomere length is closely associated with a higher risk of developing emphysema, researchers from Johns Hopkins University revealed in the American Journal of Respiratory and Critical Care Medicine.
A telomere is a protein structure at the end of a chromosome. It is a specialized structure involved in the stability and replication of the chromosome - it protects the chromosome tip from degradation. The researchers describe telomeres as the body's own cellular clocks.
Mary Armanios, MD, assistant professor of oncology, said:
"We found that in mice that have short telomeres, there was a significant increased risk of developing emphysema after exposure to cigarette smoke."
Although telomere length is genetically determined, they gradually get shorter with cell division. Shortened telomeres are seen as a sign of ageing in cells.
Dr. Armanios added:
"With age, short telomeres accumulate and cause cells to stop dividing. Telomeres can be thought of as 'biological clocks'. We wanted to determine whether telomere length itself was why susceptibility to emphysema increases with age."
Dr. Armanios and team set out to determine what the role of telomeres might be in lung disease. They studied mice with shortened telomeres and exposed them to cigarette smoke for six hours daily, five days per week for a total of six months.
They then assessed the mice's pulmonary function by analyzing lung tissue.
Dr. Armanios said:
"Although the mice had no lung disease at baseline, after exposure to cigarette smoke, they surprisingly developed emphysema. In contrast, mice with long telomeres did not develop lung disease during our experiments."
When a patient has emphysema, the small air sacs in the lungs where oxygen exchange occurs - the alveoli - are permanently lost. Emphysema tends to affect older people. Even those who have never smoked may develop it. However, the majority of sufferers are smokers or were long-term regular smokers.
Emphysema is among the top ten causes of premature death in the USA, and a common cause of disability.
Even though we know that smoking is the main risk factor, scientists are uncertain why some individuals are more susceptible to developing emphysema than others.
Unless the patient has a lung transplant, the condition is irreversible and incurable.
Dr. Armanios said:
"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. 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."
Hopefully, these new findings may eventually lead to ways of preserving lung function as humans get older, Dr. Armanios said.
"It's important to remember that there is no good reason to smoke and the best way to prevent emphysema is to stop smoking."
Dr. Armanios and team had already demonstrated that shortened telomeres cause idiopathic pulmonary fibrosis (IPF). Some IPF patients also have emphysema - especially older ones and those who smoke. Dr. Armanios added:
"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."
The authors say additional research is needed to show that the same as happened with mice also occurs in humans.
"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."
"Telomere Length is a Determinant of Emphysema Susceptibility"
Jonathan K Alder, Nini Guo, Frant Kembou, Erin M Parry, Collin J Anderson, Amany I Gorgy, Michael F Walsh, Thomas Sussan, Shyam Biswal, Wayne Mitzner, Rubin M Tuder, and Mary Armanios
Am. J. Respir. Crit. Care Med. 2011, doi:10.1164/rccm.201103-0520OC
Written by Christian Nordqvist