A Johns Hopkins University study finds that telomeres—the body’s own cellular clocks—may be a crucial factor underlying the development of emphysema. The study appears in 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.
“With age, short telomeres accumulate and cause cells to stop dividing. Telomeres can be thought of as ‘biological clocks,’” said Mary Armanios, MD, assistant professor of oncology at the Johns Hopkins School of Medicine. “We wanted to determine whether telomere length itself was why susceptibility to emphysema increases with age.”
For the study, the research team exposed mice to cigarette smoke for 6 hours a day, 5 days a week for 6 months. The researchers then analyzed the lung tissue and pulmonary function of the mice. They found that although the mice [with short telomeres] had no lung disease at baseline, after exposure to cigarette smoke, they developed emphysema. In contrast, mice with long telomeres did not develop lung disease during the study.
“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,” said Armanios. “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.”
Source: American Thoracic Society
