• Kazutetsu Aoshiba.
• First Department of Medicine, Tokyo Women' s Medical University.
• Nippon Rinsho. 2007 Apr 1; 65 (4): 629-32.

AbstractChronic obstructive pulmonary disease (COPD) is a cigarette smoking-related disorder characterized by chronic inflammation of the airways and progressive destruction of lung parenchyma, leading to airway remodeling and pulmonary emphysema. Several mechanisms have been proposed to be involved in the pathogenesis of pulmonary emphysema, including an imbalance of proteases and antiproteases, and oxidative stress. In addition to these mechanisms, recent studies suggest another mechanism involved in the development of pulmonary emphysema: apoptosis of alveolar wall cells. There is an increase in apoptotic alveolar epithelial and endothelial cells in the lungs of patients with emphysema, and since this is not counterbalanced by an increase in proliferation of alveolar wall cells as they become senescent, the net result is loss of alveolar unit leading to the development of emphysema. Studies with animal models suggest that caspases, vascular endothelial growth factor (VEGF) deficiency, oxidants, ceramide, CD8+ T-lymphocytes, elastases, and interferon-gamma may be responsible for the induction of apoptosis of alveolar wall cells. Furthermore, defective clearance of apoptotic cells in the lungs of patients with emphysema may promote inflammation. In this review, recent data on the role of apoptosis in emphysema from both animal models as well as from studies on human subjects will be discussed.

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