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There is growing evidence of higher prevalence of chronic obstructive pulmonary disease (COPD) in the elderly. Age-associated changes in the structure and function of the lung may increase a pathogenetic susceptibility to COPD. The lung may directly develop COPD in old age. Suitable animal models are required to test this hypothesis. Senescence-accelerated mice (SAM), Klotho gene depleted mice, and SMP-30 knockout mice were investigated with their short lifespan associated with premature aging in systemic organs. The structural and physiological changes demonstrated senile lung, not emphysema, without alveolar wall destruction. Tobacco smoke exposure resulted in the development of emphysema. These findings support the hypothesis that premature aging is not the direct cause of emphysema, but that premature aging enhances the susceptibility of the lung to extrinsic insults including tobacco smoke in these animal models. The mechanism of this enhancement needs further investigation and its elucidation should advance COPD management.
Yoshinosuke Fukuchi (Tue,) studied this question.