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ADVANCE Perspective: Respiratory Views

Researchers: Short Telomeres Increased Risk of Emphysema in Mice

Published July 17, 2011 11:03 PM by Sharlene George

While smoking cigarettes is the most common risk factor for emphysema, it is not known why some people are more prone to developing the disease than others.

Researchers from Johns Hopkins University suggest that telomeres, the body’s own cellular clocks, may be a crucial factor underlying the development of emphysema, according to a press release issued by the American Thoracic Society.

“We found that in mice that have short telomeres, there was a significant increased risk of developing emphysema after exposure to cigarette smoke,” said Mary Armanios, MD, assistant professor of oncology at the Johns Hopkins School of Medicine.

The study appears online ahead of the print edition of the American Journal of Respiratory and Critical Care Medicine.

Telomeres are DNA protein structures that protect chromosome ends from degradation. Their length is genetically determined, but they also shorten progressively with cell division. Short telomeres are considered one marker of aging in cells.

Dr. Armanios and her colleagues examined the role of telomeres in lung disease by studying mice that have shortened telomeres. The mice were exposed to cigarette smoke for six hours a day, five days a week for six months. After exposure to cigarette smoke, they surprisingly developed emphysema. In contrast, mice with long telomeres did not develop lung disease.

“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,” Dr. Armanios said. “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.

Previously, Dr. Armanios and her group had shown that shortened telomeres cause idiopathic pulmonary fibrosis. 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.

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