In a new study, a research team based at Brown and Yale implicates a specific mitochondrial protein and pathway in the development of COPD from exposure to cigarette smoke. Observations in human patients and experiments in mouse models show that suppression of the protein is a major cigarette-induced signature of the emphysema—lung destruction—that is seen in COPD.

“This is a new school of thought in terms of what causes emphysema and a new school of thought regarding how cigarette smoke does what it does,” said pulmonologist Dr Jack A. Elias, dean of medicine and biological sciences at Brown University and corresponding author of the study in the Journal of Clinical Investigation. “We’re showing that a lot of what’s going on is related to mitochondria.”