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There is a growing realization that COPD, or at least emphysema, involves several processes presenting in aging and cellular senescence. Endothelial progenitor cells (EPCs) contribute to neovascularization and play an important role in the development of COPD. The gene for p16 Ink4a is a major dominant senescence one. The aim of the present study was to observe changes in lung function, histomorphology of lung tissue, and expression of p16 Ink4a in lung tissue and bone marrow-derived EPCs in emphysematous mice induced by cigarette-smoke extract (CSE), and further to search for a potential candidate agent protecting against emphysema induced by CSE.

5-Aza-2&#39;-deoxycytidine protects against emphysema in mice via suppressing p16<sup>Ink4a</sup> expression in lung tissue

5-Aza-2'-deoxycytidine protects against emphysema in mice via suppressing p16<sup>Ink4a</sup> expression in lung tissue