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
ROLE OF CELLULAR SENESCENCE AND IMPAIRED INTRACELLULAR DEGRADATION PATHWAYS IN THE PATHOGENESIS OF CHRONIC OBSTRUCTIVE PULMUNARY DISEASE (COPD)
NUCERA, Francesco
2026-01-01
Abstract
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 stressPubblicazioni consigliate
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