Is COPD in adulthood really so far removed from early development?

Abstract

Chronic obstructive pulmonary disease (COPD), including chronic bronchitis and emphysema, is commonly thought of as an adult onset lung disease most often seen in aging people with a tobacco smoking history 1. Yet, conversely, only ∼20% of cigarette smokers develop full-blown emphysema, while COPD may also be seen in nonsmokers. Therefore, genetic susceptibility is a hot topic in recent COPD research. A wealth of information has been accumulating regarding genetic polymorphisms and the incidence and severity of COPD in patients. However, the mechanisms by which these genetic alterations contribute to COPD pathogenesis are as yet barely understood. Accumulated research evidence from gene knockout and transgenic mouse models suggest that some of these genetic mutations may affect lung developmental processes in early life, which may later function as an antecedent of apparently adult onset COPD. For example, conventional gene knockout of latent transforming growth factor-β binding protein 4 or Smad3 results in retarded lung alveogenesis during early postnatal life with further subsequent alveolar enlargement 2, 3 …