ROLE OF CELLULAR SENESCENCE AND IMPAIRED INTRACELLULAR DEGRADATION PATHWAYS IN THE PATHOGENESIS OF CHRONIC OBSTRUCTIVE PULMUNARY DISEASE (COPD)

COPD is currently hypothesized to be a disease of accelerated lung aging as the cells of the lower airways of these patients show several features of cellular aging: for example shortening of telomeres and damage to DNA (deoxyribonucleic acid), cellular senescence, activation of Intracellular signalling pathway mediated by phosphatidyl-inositol-3-kinase and the mammalian target of rapamycin (PI3K-mTOR), autophagy impairments, mitochondrial disorders, stem cell depletion, microRNA profile impairment, immunosenescence, chronic inflammation (inflammaging), associated with a decrease in the expression of anti-aging molecules such as sirtuins (SIRTs). Many of these processes are activated by oxidative stress