PMC:7565665 / 61308-63224 JSONTXT

{"target":"http://pubannotation.org/docs/sourcedb/PMC/sourceid/7565665","sourcedb":"PMC","sourceid":"7565665","source_url":"https://www.ncbi.nlm.nih.gov/pmc/7565665","text":"Our relatively recent study using GSNO, an endogenously occurring nitric oxide donor, highlights the biological significance of CS-induced CFTR dysfunction-related autophagy impairment in mediating COPD-emphysema pathogenesis. We showed that an augmentation of GSNO decreases cigarette smoke extract (CSE)-induced ROS activation and autophagy-flux impairment by rescuing the aggresome-bound perinuclear CFTR to the PM [62]. Furthermore, using a preclinical COPD-emphysema murine model, we demonstrated that chronic CS (Ch-CS) induced an increase in inflammatory cytokines in BALF, aggresome formation, CFTR-aggresome localization, oxidative/nitrosative stress, and apoptosis, and the emphysematous changes (alveolar airspace enlargement) were significantly improved by augmenting the airway GSNO levels [62]. Thus, this study provides proof-of-concept evidence that GSNO augmentation could be further tested as a potential strategy to correct CS-induced CFTR-autophagy defects. Apart from cysteamine and GSNO, we also tested the potential of other FDA-approved autophagy-inducing drugs, such as gemfibrozil (GEM), which induces lysosome formation, and fisetin, in controlling CS-induced autophagy dysfunction and hampered pathogen clearance. Our study showed that CS/CSE-induced TFEB/autophagy impairment, inflammatory-oxidative stress, apoptosis, and senescence can be mitigated by treatment with GEM/fisetin via TFEB induction [34]. In a subsequent investigation, we demonstrated that CSE-induced autophagy dysfunction in macrophages is a critical mechanism of phagocytosis defects and the resulting diminished clearance of P. aeruginosa [33,35]. The autophagy-inducing antioxidant fisetin was able to restore the CS-induced phagocytosis defect and facilitate P. aeruginosa clearance [35], suggesting the potential of autophagy-inducing strategies in controlling exacerbations prevalent in COPD-emphysema 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