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- W3205582645 abstract "Chronic obstructive pulmonary disease (COPD),1 a representative aging-related pulmonary disorder, is mainly caused by cigarette smoke (CS) exposure. Age is one of the most important risk factors for COPD development, and increased cellular senescence in tissues and organs is a component of aging. CS exposure can induce cellular senescence, as characterized by irreversible growth arrest and aberrant cytokine secretion of the senescence-associated secretory phenotype; thus, accumulation of senescent cells is widely implicated in COPD pathogenesis. CS-induced oxidative modifications to cellular components may be causally linked to accelerated cellular senescence, especially during accumulation of damaged macromolecules. Autophagy is a conserved mechanism whereby cytoplasmic components are sent for lysosomal degradation to maintain proteostasis. Autophagy diminishes with age, and loss of proteostasis is one of the hallmarks of aging. We have reported the involvement of insufficient autophagy in regulating CS-induced cellular senescence with respect to COPD pathogenesis. However, the role of autophagy in COPD pathogenesis can vary based on levels of cell stress and type of selective autophagy because excessive activation of autophagy can be responsible for inducing regulated cell death. Senotherapies targeting cellular senescence may be effective COPD treatments. Autophagy activation could be a promising sonotherapeutic approach, but the optimal modality of autophagy activation should be examined in future studies." @default.
- W3205582645 created "2021-10-25" @default.
- W3205582645 creator A5024974883 @default.
- W3205582645 creator A5040461128 @default.
- W3205582645 date "2022-01-01" @default.
- W3205582645 modified "2023-10-14" @default.
- W3205582645 title "Cellular senescence—an aging hallmark in chronic obstructive pulmonary disease pathogenesis" @default.
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