The ability to prevent the oxidative damage to the lung tissue and the potential to regenerate injured cells are two key determinants of aging [84]. While still an area of controversy, reports indicate that exposure to cigarette smoke, ROS, and other environmental stressors may accelerate biological processes associated with normal aging [85, 86]. Moreover, recent epidemiological study has suggested that about half of patients with COPD fail to achieve full lung function in adolescence and early adulthood. In these individuals, this disease might develop as a consequence of the “normal” decline in lung function with age. Similar to emphysema, lung aging is characterized by a decrease in the density and an increase in the diameter of the membranous bronchioles. However, unlike emphysema, there are no differences in alveolar attachments. COPD may represent an accelerated (or normal) form of lung aging.
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