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Like other organs, the lungs also age, manifesting degenerative changes during aging. At the cellular level, age-related deterioration in the lungs includes the depletion of stem cell pool, increased oxidative stress and accumulated DNA damages leading to telomere shortening and mitochondrial dysfunction (Sahin et al., 2011). As a global phenomenon in the lung, aging affects various cell types, including epithelial, endothelial, mesenchymal and immune cells.

            The lung harbors distinct stem cell populations which reside in the supporting niches to maintain tissue homeostasis and respond to injury (Kim et al., 2005a; Rawlins et al., 2009a; Rock et al., 2009a; Barkauskas et al., 2013a; Hogan et al., 2014; Vaughan et al., 2014; Jain et al., 2015a). During aging, the number and function of lung stem cells decline and gradually lose their regenerative capacity. Age-related replicative exhaustion, depletion of stem cell pool, and alterations in stem cell niches result in lung dysfunction. Growing evidence reveals that the dysfucntion of epithelial cell populations is a key component of the aging process. For instance, a recent study showed age-associated changes in the cellular composition, organization and local microenvironment of the mouse tracheal epithelium. They found that the number and proportion of basal cells in the airways of aged mice decreased and the appearance of age-associated gland-like structures (ARGLS) in the submucosa may due to a response to chronic changes in the microenvironment (Wansleeben et al., 2014).

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            Lung aging is closely associated with the development and pathogenesis of chronic respiratory diseases, of which the prevalence and diagnosis increase with age. These include chronic obstructive pulmonary disease (COPD), idiopathic pulmonary fibrosis (IPF), emphysema, submucosal gland hypertrophy and cancer (Chilosi et al., 2013; Faner et al., 2012). Studies in tissues from emphysema patients showed that the depletion of stem cell pool in aged lungs were due to the inability of turnover and increased cellular senescence, resulting in the loss of normal alveolar structures and diminished tissue regeneration (Tsuji et al., 2006; Yokohori et al., 2004). Telomere shortening, cellular senescence and stem cell exhaustion, have been found to be closely associated with the development of IPF. For instance, mutations in the enzyme telomerase and the consequential telomere shortening are involved in the pathogenesis of both familial and sporadic IPF, which also link to the development of COPD and emphysema (Alder et al., 2011; Armanios et al., 2007). Furthermore, age also causes extracellular changes in the lung that influence the activation of signaling pathways of proliferation, differentiation and senescence in the seeded cells (Sokocevic et al., 2013). Overall, aging alters the lungs at both cellular and extracellular levels and these age-associated changes cause tissue dysfunction and the development of chronic pulmonary disorders.

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