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To reach that conclusion, the investigators compared lung fibroblasts (a type of cell) taken from nonsmokers without lung disease and patients with a heavy smoking history and severe emphysema. Fibroblasts from the smokers with emphysema had lost their ability to divide or grow, confirming that smoking habits cause cell aging. The cells also had lower levels of Werner's syndrome protein, compared to cells from nonsmokers.

The team also applied cigarette smoke extract to cultured lung fibroblasts taken from nonsmokers. They saw that Werner's syndrome protein expression was decreased, and the cells had lost their ability to repair wounds. In contrast, when the team caused the lung fibroblasts in petri dishes to overexpress Werner's syndrome protein, it had a protective effect and helped resist the damaging effects of cigarette smoke.

"Overall, our study may support efforts to target Werner's syndrome protein for use in developing treatments for smoking-related conditions such as emphysema," Nyunoya said.

The team will next use mouse models to further study the effects of smoking on Werner's syndrome protein.