Kurniawan FD, Andarini SL, Yunus F. J Respir Indones. 2011;31(4):224-32.

Abstract
Chronic Obstructive Pulmonary Disease (COPD) prevalence in the elderly is increasing. During aging, lung structure and function deteriorate and increase pathogenetic susceptibility to COPD. Aging is a progressive decline of homeostasis that occurs after the reproductive phase of life is complete and leading to an increasing risk of disease or death. Failure of organs to repair DNA damage by oxidative stress and telomere shortening as a result of repeated cell division contribute to aging. Cellular senescence is a state of irreversible growth arrest induced either by telomere shortening (replicative senescence) or by telomere-independent signals (stress-induced premature senescence). Cellular damage caused by aging and cigarette smoking induces apoptosis and it increases cell cycle turnover as a compensatory. In addition, aging and smoking cause cellular senescence and cause cellular proliferation to stop. This apoptosis-proliferation imbalance leads to blocked tissue regeneration, alveolar cells declining and emphysematous lesions progression fnally. This literature review will discuss aging and cellular senescence role in COPD pathogenesis.
Key words: chronic obstructive pulmonary disease; aging; cellular senescence; telomere; apoptosis; proliferation

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