Abstract
Chronic obstructive pulmonary disease (COPD) is a chronic inflammatory airway disease. It has become one of the commonest diseases worldwide and a major global healthcare problem. The disease progresses very slowly and, in contrast to asthma, the majority of affected patients are middle-aged or elderly. There is increasing evidence of a direct relationship between aging and an increased incidence of chronic inflammatory disease. Thus, in this review, the link between aging of the lung and the progression of COPD is discussed. Aging, or senescence, is defined as the progressive decline in homeostasis that occurs after the reproductive phase of life is completed, leading to an increasing risk of disease or death. This is the result of a failure of organ maintenance resulting from DNA damage, oxidative stress and telomere shortening. During aging, pulmonary function progressively deteriorates and inflammation of the lung increases, and these changes are accompanied by structural changes. Environmental stimulation, for example as a result of cigarette smoke or other pollutants, may accelerate aging of the lung (model 1) or worsen aging-related events in the lung (model 2), and this consequently induces further progress of COPD. Recent studies of anti-aging molecules have provided new insights into the molecular mechanism of the pathophysiology of COPD.