Roles of apoptosis, cell senescence, and DNA damage in the pathogenetic mechanism of COPD
Aoshiba, K.
Nihon Rinsho. Japanese Journal of Clinical Medicine 69(10): 1754-1757
2011
ISSN/ISBN: 0047-1852 PMID: 22073568 Document Number: 655021
Pulmonary emphysema is a dynamic phenomenon involving not only the gradual destruction of extracellular matrix by excess of proteases, but also apoptosis, cell proliferation, and senescence. Cellular proliferation compensates for enhanced alveolar cell apoptosis whereas cell senescence caused by cigarette smoking and increased cell turnover halts cell proliferation, tipping the balance toward apoptosis. As a result, alveolar cells gradually disappear and emphysematous lesions advance. At the same time, cellular senescence causes chronic inflammation through enhanced production of proinflammatory cytokines. Recent findings suggest that DNA damage (double strand breaks) underlies the molecular mechanisms of apoptosis, cell senescence, and chronic inflammation in emphysematous lungs.