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Peranan Penuaan dan Senescence Selular dalam Patogenesis PPOK
Chronic Obstructive Pulmonary Diseases (COPD) pervelence in the elderly is incresing. During aging, lung structure and function deteriorate and increase pathogenetic susceptibility to COPD. Aging is a progressive decline of homeostasis that occus after the reproductive phase of life is complete and leading to an increasing risk of disease of death. Failure of organs to repair DNA damage by oxidative stress and telomere shorting as a result of repeated cell division contribute to aging. Cellular senescence is a state of irreversible growth arrest inducted either by teleomere shortening (replicative sencescence) or by telomere independent signals (stress-inducted premature-independent signals (stresspinducted 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 renescence and cause cellular proliferation to stop. This apoptosis-proliferation imbalance leads to blocked tissue regeneration, alveolar cells declining and emphysemators lesions progression finally. This literature review will descuss aging and cellular senescence role in COPD pathogenesis
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